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Unicellular and multicellular Organisms are best explained through design

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Unicellular and multicellular Organisms are best explained through design

One of the central problems of biology is the emergence of complexity. How did complex multicellular organisms emerge, and how is genetic information translated to a spatially organized body plan? The hallmark of a developing multicellular organism is the fact that decisions regarding cell fate are not taken at the level of the individual cell. To allow the building of complex organs with intricate patterns of cellular specialization, such decisions are taken at the population level in a cell-nonautonomous manner. A breakthrough in the elucidation of the genetic control of such intercellular communication in developmental patterning events was made by Nüsslein-Volhard and Wieschaus. 8

Proponents of evolution claim like a mantra, that microevolution leads to macroevolution, and no barrier exists which hinders the transition from one to the other, which last not least explains our biodiversity today.

The emergence of multicellularity was supposedly, a major evolutionary leap. Indeed, most biologists consider it one of the most significant transitions in the evolutionary history of Earth’s inhabitants. “How a single cell made the leap to a complex organism is, however, one of life’s great mysteries.”

Macroevolutionary scenarios and changes include major transitions, that is from LUCA, the last common universal ancestor, to the congregation to yield the first prokaryotic cells, the associations of prokaryotic cells to create eukaryotic cells with organelles such as chloroplasts and mitochondria, and the establishment of cooperative societies composed of discrete multi-cellular individuals. Or in other words: The current hierarchical organization of life reflects a series of transitions in the units of evolution, such as from genes to chromosomes, from prokaryotic to eukaryotic cells, from unicellular to multicellular individuals, and from multi-cellular organisms to societies. Each of these steps requires the overcome of huge hurdles and increase of complexity, which can only be appreciated by the ones, that have to spend time to educate themselves, and gained insight of the extraordinarily complex and manifold mechanisms involved. The emergence of multi-cellularity was ostensibly a major evolutionary leap. 

The switch from single-celled organisms to ones made up of many cells have supposedly evolved independently more than two dozen times.  Evolution requires more than a mere augmentation of an existing system for co-ordinated multicellularity to evolve; it requires the ex nihilo creation of an entirely new system of organization to coordinate cells appropriately to form a multicellular individual.

There is a  level of structure found only in multicellular organisms: intercellular co-ordination. The organism has strategies for arranging and differentiating its cells for survival and reproduction. With this comes a communication network between the cells that regulate the positioning and abundance of each cell type for the benefit of the whole organism. A fundamental part of this organization is cellular differentiation, which is ubiquitous in multicellular organisms. This level cannot be explained by the sum of the parts, cells, and requires coordination from an organizational level above what exists in individual cells. There is a 4-level hierarchy of control in multicellular organisms that constitute a gene regulatory network. This gene regulatory network is essential for the development of the single cell zygote into a full-fledged multicellular individual.

If evolution and transition from unicellular to multicellular life is exceedingly complex, the chance that it happened once is also exceedingly small. That it happened multiple times separately, becomes even more remotely possible. Convergent evolution of similar traits is evidence against, not for evolution. In order to infer that a proposition is true, these nuances are important to observe. The key is in the details. As Behe states: In order to say that some function is understood, every relevant step in the process must be elucidated. The relevant steps in biological processes occur ultimately at the molecular level, so a satisfactory explanation of a biological phenomenon such as the de novo make of cell communication and cell junction proteins essential for multi-cellular life must include a molecular explanation.

The cells had not only to hold together, but important mechanisms to stick the cells together had to emerge, that is, the ability of individual cells to associate in precise patterns to form tissues, organs, and organ systems requires that individual cells be able to recognize, adhere to, and communicate with each other.

Of all the social interactions between cells in a multicellular organism, the most fundamental are those that hold the cells together. The apparatus of cell junctions and the extracellular matrix is critical for every aspect of the organization, function, and dynamics of multicellular structures. Animal cells use specialized adhesion receptors to attach to one another. Many of these adhesion proteins are transmembrane proteins, which means the extracellular portion of these proteins can interact with the extracellular portion of similar proteins on the surface of a neighboring cell. Although diagrams of adhesive structures may suggest that they are static once assembled, they are anything but. Cells can dynamically assemble and disassemble adhesions in response to a variety of events.  This seems to be an essential requirement for function right from the beginning of multicellularity.  Many adhesion proteins are continuously recycled: Protein at the cell surface is internalized by endocytosis, and new protein is deposited at the surface via exocytosis. The molecular machines to exercise these functions, therefore, had to emerge together with adhesion proteins. Furthermorecell adhesion is coordinated with other major processes, including 

1.cell signaling, 
2.cell movement, 
3.cell proliferation, and 
4.cell survival. 

We now know that cell-cell adhesion receptors fall into a relatively small number of classes. They include 

1.immunoglobulin superfamily (IgSF) proteins, 
3.selectins, and, in a few cases, 

In order to explain multicellularity, its origin must be explained.

Thus, the apparatus of cell junctions and the extracellular matrix is critical for every aspect of the organization, function, and dynamics of multicellular structures. The arise of adhesive junctions, tight junctions and gap junctions,  and how they emerged is, therefore, a key factor to explain multi-cellular life. The cells of multi-cellular organisms detect and respond to countless internal and extracellular signals that control their growth, division, and differentiation during development, as well as their behavior in adult tissues. At the heart of all these communication systems are regulatory proteins that produce chemical signals, which are sent from one place to another in the body or within a cell, usually being processed along the way and integrated with other signals to provide clear and effective communication. The rise of these communication channels had to arise together with junction mechanisms in order to establish successful multicellular organisms. One feature without the other would not have provided success and advantage of survival. 

The ability of cells to receive and act on signals from beyond the plasma membrane is fundamental to life.  This conversion of information into a chemical change, signal transduction, is a universal property of living cells. Signal transductions are remarkably specific and exquisitely sensitive. Specificity is achieved by precise molecular complementarity between the signal and receptor molecules. 

Question: signal transduction had to be present in the first living cells. How could the specificity of the signal molecule, and the precise fit on its complementary receptor have evolved ? or the Amplification, or the desensitization/adaptation, where the receptor activation triggers a feedback circuit that shuts off the receptor or removes it from the cell surface, once the signal got trough? 

Three factors account for the extraordinary sensitivity of signal transducers: the high affinity of receptors for signal molecules, cooperativity (often but not always) in the ligand-receptor interaction, and amplification of the signal by enzyme cascades. The trigger for each system is different, but the general features of signal transduction are common to all: a signal interacts with a receptor; the activated receptor interacts with cellular machinery, producing a second signal or a change in the activity of a cellular protein; the metabolic activity of the target cell undergoes a change; and finally, the transduction event ends. This seems to be an irreducible system, requiring high content of pre-programming and advanced coding.

Question: how did the high affinity, cooperativity, and amplification have emerged? Is a preestablished convention not necessary, and so a mental process to yield the function? Is trial and error or evolution not a completely incapable mechanism to get this functional information system? 

This is an important, essential and fundamental macroevolutionary change, and the explanation of macro-evolution must account for these changes, and provide feasible possible and likely ways through mutation and natural selection. Beside this,  a shift on several levels of biological organization had to occur, providing a considerable advantage of survival, considering that for example  one of the first cooperative steps required for the evolution of multicellularity in the volvocine algae was the development of the extracellular cell matrix from cell wall components, which can be metabolically costly to produce. But much more is required.

Ann Gauger: New genes and proteins must be invented. The cytoskeleton, Hox genes, desmosomes, cell adhesion molecules, growth factors, microtubules, microfilaments, neurotransmitters, whatever it takes to get cells to stick together, form different shapes, specialize, and communicate must all come from somewhere. Regulatory proteins and RNAs must be made to control the expression in time and space of these new proteins so that they all work together with existing pathways.In fact, in order for development to proceed in any organism, a whole cascade of coordinated genetic and biochemical events is necessary so that cells divide, change shape, migrate, and finally differentiate into many cell types, all in the right sequence at the right time and place. These cascades and the resulting cell divisions, shape changes, etc., are mutually interdependent. Interrupting one disrupts the others.

And last not least: 

Like engineers carefully blowing up a bridge, cells have intricate, programmed suicide mechanisms. Without apoptosis, all multicellular life would be impossible. Good luck to proponents of evolution to explain how it emerged........

Transition from from Unicellular to Multicellular Organisms

It is now widely accepted, on the basis of structural, biochemical, and molecular evidence, that the five major types of large, complex, multicellular organisms (i.e., red algae, brown algae, land plants, fungi, and animals) arose separately from different types of unicellular ancestors.

The evolution of multicellular life from simpler, unicellular microbes was a pivotal moment in the history of biology on Earth and has drastically reshaped the planet’s ecology. However, one mystery about multicellular organisms is why cells did not return back to single-celled life. 2

In the beginning there were supposedly single cells. Today, many millions of years later, most plants, animals, fungi, and algae are composed of multiple cells that work collaboratively as a single being. Despite the various ways these organisms achieved multicellularity, their conglomeration of cells operate cooperatively to consume energy, survive, and reproduce. But how did multicellularity evolve? Did it evolve once or multiple times? How did cells make the transition from life as a solo cell to associating and cooperating with other cells such that they work as a single, cohesive unit? 3

What we usually teach when discussing the origin and evolution of metazoans in geology class is that single-celled eukaryotes (organisms with a nucleus) like choanoplagellates learned how to clump together and chemically communicate to form sponges - thought to be one of the earliest multicellular organisms.4

While evolutionists can provide plenty of guesses about how multicellular organisms could have evolved from unicellular organisms, the fact is evolutionists have no idea how they actually evolved. And if evolutionists have no idea how they evolved, can we really be sure that they did evolve? Evolutionists scoff at such skepticism. It is unwarranted, they say, because evolution is a fact. 6

This transition is probably the easiest to understand.

Several colonial flagellated green algae provide a clue. These species are called colonial because they are made up simply of clusters of independent cells. If a single cell of Gonium, Pandorina, or Eudorina is isolated from the rest of the colony, it will swim away looking quite like a Chlamydomonas cell. Then, as it undergoes mitosis, it will form a new colony with the characteristic number of cells in that colony.

(The figures are not drawn to scale. Their sizes range from Chlamydomonas which is about 10 µm in diameter — little larger than a human red blood cell — to Volvox whose sphere is some 350 µm in diameter — visible to the naked eye.)

The situation in Pleodorina and Volvox is different. In these organisms, some of the cells of the colony (most in Volvox) are not able to live independently. If a nonreproductive cell is isolated from a Volvox colony, it will fail to reproduce itself by mitosis and eventually will die. What has happened? In some way, as yet unclear, Volvox has crossed the line separating simple colonial organisms from truly multicellular ones. Unlike Gonium, Volvox cannot be considered simply a colony of individual cells. It is a single organism whose cells have lost their ability to live independently. If a sufficient number of them become damaged, the entire sphere of cells will die.

What has Volvox gained? In giving up their independence, the cells of Volvox have become specialists. No longer does every cell carry out all of life's functions (as in colonial forms); instead certain cells specialize to carry out certain functions while leaving other functions to other specialists. In Volvox this process goes no further than having certain cells specialize for reproduction while others, unable to reproduce themselves, fulfill the needs for photosynthesis and locomotion.

In more complex multicellular organisms, the degree of specialization is carried much further. Each cell has one or two precise functions to carry out. It depends on other cells to carry out all the other functions needed to maintain the life of the organism and thus its own.

The specialization and division of labor among cells is the outcome of their history of differentiation. One of the great problems in biology is how differentiation arises among cells, all of which having arisen by mitosis, share the same genes. Link to a discussion of the solution.

The genomes of both Chlamydomonas and Volvox have been sequenced. Although one is unicellular, the other multicellular, they have not only about the same number of protein-encoding genes (14,516 in Chlamydomonas, 14,520 in Volvox) but most of these are homologous. Volvox has only 58 genes that have no relatives in Chlamydomonas and even fewer unique mRNAs.

At one time, many of us would have expected that a multicellular organism like Volvox with its differentiated cells and complex life cycle would have had many more genes than a single-celled organism like Chlamydomonas. But that turns out not to be the case.
How to explain this apparent paradox? My guess is that just as we have seen in the evolution of animals [Examples], we are seeing here that the evolution of organismic complexity is not so much a matter of the evolution of new genes but rather the evolution of changes in the control elements (promoters and enhancers) that dictate how and where the basic tool kit of eukaryotic genes will be expressed .

The evidence is compelling that all these organisms are close relatives; that is, belong to the same clade. They illustrate how colonial forms could arise from unicellular ones and multicellular forms from colonial ones.

The Origin of Multicellularity 5

From an evolutionary perspective, support for the transition from unicellular (single cell) to multicellular organisms requires the emergence of several novel biochemical systems. Such systems include:

pathways that transform cells from generalized to specialized forms during growth and development;
mechanisms for the migration of cells relative to each other during growth and development;
structures that support cell-cell adhesions;
and mechanisms for cell-cell communication.
All of these systems have to be in place and operate in an integrated fashion to support multicellularity.

The Origin of Multicellularity in Brown Algae

To gain understanding about how multicellularity originated in brown algae, a research consortium sequenced the entire genome (consisting of 214 million genetic letters) of the brown algae Ectocarpus siliculosus. They then compared it to closely related unicellular organisms. The research team noticed that multicellularity’s origin in the brown algae appears to correlate with the appearance of a rich ensemble of genes that encode proteins involved in signal transduction (processes that support cell-cell communication).

They also noted that this same collection of genes also correlates with the advent of multicellularity in plants and animals. According to the evolutionary paradigm, multicellularity arose independently in brown algae, plants, and animals. And the same biochemical systems that make multicellularity possible also appear to have arisen in each group of organisms on three separate occasions.

Implications for the Evolutionary Paradigm

Evolutionary processes are blind and undirected. Their very essence renders evolutionary outcomes unpredictable and nonrepeatable. According to the concept of historical contingency, espoused by late scientist Stephen Jay Gould in his book Wonderful Life, chance governs biological and biochemical evolution at its most fundamental level. Evolutionary pathways consist of a historical sequence of chance genetic changes operated on by natural selection, which also consists of chance components. Thus, if evolutionary events could be “rewound” and “replayed,” the outcome would be dramatically different every time. The inability of evolutionary processes to retrace the same path makes it highly unlikely that the same biological and biochemical designs would appear repeatedly throughout nature among unrelated organisms.

Yet it looks as if evolution has repeated itself, time and time again! Evolutionary biologists note that evolutionary processes frequently seem to converge independently on identical anatomical, physiological, behavioral, and biochemical systems. (As a case on point, go here and here to see two articles I wrote on this phenomenon some time ago.) Evolutionary biologists refer to repeated evolutionary outcomes as convergence.

In my book The Cell’s Design I document over one hundred examples of convergence at the biochemical level. On this basis I argue that if historical contingency truly reflects the nature of evolutionary processes, then the widespread occurrence of a broad range of biochemical systems emerging repeatedly raises significant questions about the validity of evolutionary explanations for life’s origin and diversity.

The repeated origin of multicellularity in brown algae, plants, and animals defies an evolutionary explanation, particularly since it involves the independent origin of virtually the same biochemical systems. But this new insight makes sense if a Creator responsible for the multi-member church was also responsible for assembling multicellular life-forms.

Birds and bats belong to different groups, with birds assigned to the class Aves and bats to the class Mammalia. 4According to the evolutionary paradigm, undirected natural processes yielded the identical outcome (wings, in this case) because the forces of selection channeled evolutionary pathways to the same endpoint.

This explanation doesn’t square up, however. If biological systems are the product of evolution, then the same biological systems should not recur throughout nature. Chance governs biological and biochemical evolution at its most fundamental level. Evolutionary pathways consist of a historical sequence of chance genetic changes operated on by natural selection, which, too, consists of chance components. The consequences are profound. If evolutionary events could be repeated, the outcome would be dramatically different every time. The inability of evolutionary processes to retrace the same path makes it highly unlikely that the same biological and biochemical designs should repeatedly appear throughout nature.


The Multiple Origins of Complex Multicellularity

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2 Multicellular fossils from 600 mya? on Tue May 12, 2015 2:37 pm


The Ectocarpus genome and the independent evolution of multicellularity in brown algae

Brown algae (Phaeophyceae) are complex photosynthetic organisms with a very different evolutionary history to green plants, to which they are only distantly related1. These seaweeds are the dominant species in rocky coastal ecosystems and they exhibit many interesting adaptations to these, often harsh, environments. Brown algae are also one of only a small number of eukaryotic lineages that have evolved complex multicellularity (Fig. 1) We report the 214million base pair (Mbp) genome sequence of the filamentous seaweed Ectocarpus siliculosus (Dillwyn) Lyngbye, a model organism for brown algae, closely related to the kelps6 (Fig. 1). Genome features such as the presence of an extended set of light-harvesting and pigment biosynthesis genes and new metabolic processes such as halide metabolism help explain the ability of this organism to cope with the highly variable tidal environment. The evolution of multicellularity in this lineage is correlated with the presence of a rich array of signal transduction genes. Of particular interest is the presence of a family of receptor kinases, as the independent evolution of related molecules has been linked with the emergence of multicellularity in both the animal and green plant lineages. The Ectocarpus genome sequence represents an important step towards developing this organism as a model species, providing the possibility to combine genomic and genetic approaches to explore these and othe  aspects of brown algal biology further.

The 16,256 protein coding genes present in the 214 Mbp haploid male genome of E. siliculosus are rich in introns (seven per gene on average), have long 39 untranslated regions (average size: 845 bp) and are often located very close to each other on the chromosome (29% of the intergenic regions between divergently transcribed genes are less than 400 bp long; Table 1 .

Repeated sequences, including DNA transposons, retrotransposons and helitrons, make up 22.7% of the Ectocarpus genome. Small RNAs mapped preferentially to transposons, indicating that they have a role in silencing these elements despite the absence of detectable levels of cytosinemethylation in the genome. Sequencing also revealed the presence of an integrated copy of a large DNA virus, closely related to the Ectocarpus phaeovirus EsV-1 (ref. 8; Fig. 2a).

Approximately 50% of individuals in natural Ectocarpus populations show symptoms of viral infection 9,10 but the sequenced Ectocarpus strain Ec 32 has never been observed to produce virus particles and expression analysis showed that almost all of the viral genes were silent (Fig. 2b ). The shallow waters of the intertidal region are an attractive habitat for marine, sedentary, photosynthetic organisms providing them with both a substratum and access to light. However, the shoreline is a also a hostile environment necessitating an ability to cope with tidal changes in light intensity, temperature, salinity and wave action, and with the biotic stresses characteristic of dense coastal ecosystems. Several features of the Ectocarpus genome indicate that this alga has evolved effective mechanisms for survival in this environment. For example, there is a large family of light harvesting complex (LHC) genes in Ectocarpus (53 loci, although some are probably pseudogenes), including a cluster of 11 genes with highest similarity to the LI818 family of light-stress related LHCs. The Ectocarpus genome is also predicted to encode a light-independent protochlorophyllide reductase (DPOR), allowing efficient synthesis of chlorophyll under dim light. Together these data indicate that Ectocarpus has a complex photosynthetic system that should enable against halogenated compounds produced by kelps as defence molecules 12, allowing it to grow epiphytically on these organisms 14,15. The cell walls of brown algae contain unusual polysaccharides such as alginates and fucans16, with properties that are important both in terms of resistance to mechanical stresses and as protection from predators. Analysis of the Ectocarpus genome failed to detect homologues of many of the enzymes that are known, fromother organisms, to have roles in alginate biosynthesis and in the remodelling of alginates, fucans and cellulose, indicating that brown algae have independently evolved enzymes to carry out many of these processes. However, a number of polysaccharide modifying enzymes, such as mannuronan C5 epimerases, sulphotransferases and sulphatases, were identified. These enzymes are likely to modulate physicochemical properties of the cell wall, influencing rigidity, ion exchange16 and resistance to abiotic stress. Comparison of genomes from a broad range of organisms (Fig. 3) indicated that the major eukaryotic groups have retained distinct but overlapping sets of genes since their evolution from a common ancestor, with new gene families evolving independently in each lineage.

On average, lineages that have given rise to multicellular organisms have lost fewer gene families and evolved more new gene families than unicellular lineages. However, we were not able to detect any significant, common trends, such as a tendency for the multicellular lineages to gain families belonging to particular functional (gene ontology) groups. Analysis of the gene families that are predicted to have been gained by the Ectocarpus genome since divergence from the unicellular diatoms indicated a significant gain in ontology terms associated with protein kinase activities, and these genes include a particularly interesting family of membrane-spanning receptor kinases. Receptor kinases have been shown to have key roles in developmental processes such as differentiation and cellular patterning in both the animal and green plant lineages17. Animal tyrosine and green plant serine/threonine receptor kinases form two separate monophyletic clades, indicating that these two families evolved independently, and in both lineages the emergence of receptor kinases is thought to have been a key event in the evolution of multicellularity 18,19. The Ectocarpus receptor kinases also form a monophyletic clade, discrete from those of animal and green plant receptor kinases, indicating that the brown algal family also evolved independently (Fig. 4).

The evolution of membrane-spanning receptor kinases may, therefore, have been a key step in the evolution of complex multicellularity in at least three of the five groups that have attained this level of developmental sophistication.No orthologues of the Ectocarpus receptor kinase familywere found in other stramenopile genomes, but a detailed analysis of two complete oomycete genome sequences identified a phylogenetically distinct family of receptor kinases (Fig. 4). The Ectocarpus genome contains a number of other genes that could have potentially had important roles in the development of multicellularity , although it should be noted that the functions of these proteins will need to be confirmed experimentally. For example there are several additional membrane-localized proteins of interest, including three integrin related proteins. Integrins have an important role in cell adhesion in animals 20 but integrin genes are absent from all the previously sequenced stramenopile genomes. The Ectocarpus genome also encodes a large number of ion channels, compared to other stramenopile genomes. These include several channels that are likely to be involved in calcium signalling such as an inositol triphosphate/ ryanodine type receptor (IP3R/RyR), four 4-domain voltage-gated calcium channels, and an expanded family of 18 transient receptor potential channels. Members of all these classes are found in animal genomes but are absent from the genomes of land plants 21,22. No IP3R genes have been identified in the sequenced diatom and oomycete genomes, but the presence of an IP3R in Ectocarpus is consistent with the demonstration of ‘animal-like’ fast calcium waves and inositolphosphate- induced calcium release in embryos of the brown alga Fucus serratus 23,24. The ion channels in the Ectocarpus genome illustrate how the evolutionary fates of eukaryotic lineages have probably depended not only on the evolution of new gene functions but also on the retention of genes already present in ancestral genomes. Along similar lines, there is evidence that, compared to unicellular organisms, multicellular organisms have tended to retain a more complete Rad51 family, which encodes DNA repair proteins including members with important roles during meiosis25. This is also the case in the stramenopiles, where Ectocarpus has a markedly more complete Rad51 gene family than the other sequenced members of the group . Ectocarpus also possesses a more extensive set of GTPase genes than other stramenopile genomes  and an analysis of transcription-associated proteins indicated that Ectocarpus and oomycete genomes have a broader range of transcription factor families than the unicellular diatoms. Analysis of a large set of small RNA sequences allowed the identification of 26 microRNAs in Ectocarpus. This observation, together with the identification of microRNAs in three other eukaryotic groups, the archaeplastid, opisthokont and amoebozoan lineages26, indicates that these regulatory molecules were present from an early stage of eukaryotic evolution. Sixty-seven candidate target sites were identified for 12 of the 26 microRNAs. Interestingly, 75% of these target sequences occur in genes with leucine-rich repeat (LRR) domains. The LRR genes include many members of the ROCO (Roc GTPase plus COR (C-terminal of Roc) domain) family27 that are predicted to have evolved since the split from the diatoms. Taken together, these observations indicate that a significant proportion of the microRNAs identified may regulate recently evolved processes. This is interesting in the light of suggestions that microRNAs may have had a key role in the evolution of complex multicellularity in the animal lineage 28. Analysis of the Ectocarpus genome has revealed traces both of its ancient evolutionary past and of more recent events associated with the emergence of the brown algal lineage. The former include the diverse origins of the genes that make up the genome, many of which were acquired via endosymbiotic events, whereas the latter include the recent emergence of new gene families and the evolution of an unusual genome architecture, in terms both of gene structure and organization It is likely that the evolution of complex multicellularity within brown algae depended on events spanning both timescales. The conservation of completeness and diversity within key gene families over the long term seems to have been as important as the more recent evolution of novel proteins, such as the brown algal
receptor kinase family.

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From Simple To Complex

Macroevolutionary scenarios and changes include major transitions, that is from LUCA, the last common universal ancestor, to the congregation to yield the first prokaryotic cells, the associations of prokaryotic cells to create eukaryotic cells with organelles such as chloroplasts and mitochondria, and the establishment of cooperative societies composed of discrete multi-cellular individuals. Each of these steps requires the overcome of huge hurdles and increase of complexity, which can only be appreciated by the ones, that have spend the time to educate themselves, and gained insight of the extraordinarily complex and manifold mechanisms involved. The emergence of multicellularity was ostensibly a major evolutionary leap. Indeed, most biologists consider it one of the most significant transitions in the evolutionary history of Earth’s inhabitants.

The switch from single-celled organisms to ones made up of many cells has supposedly evolved independently more than two dozen times. What can this transition teach us about the origin of complex organisms such as animals and plants? 10

Given the complexity of most organisms—sophisticated embryogenesis, differentiation of multiple tissue types, intricate coordination among millions of cells—the emergence of multicellularity was ostensibly a major evolutionary leap. Indeed, most biologists consider it one of the most significant transitions in the evolutionary history of Earth’s inhabitants. But single-celled organisms have stuck together or assembled to spawn multicellular descendants more than two dozen times, suggesting that maybe it’s not such a big leap after all.

“The transition from unicellularity to multicellularity is critical for explaining the diversity of life on Earth,” says evolutionary biologist Casey Dunn of Brown University. “We tend to think of it as quite special, but maybe it’s not. Maybe this is an easier transition than we think.”

To understand how and why it happened, scientists are utilizing the recent explosion in genomics data to assemble more accurate phylogenies and piece together each step in the transition to multicellular life. Despite their efforts, however, the origins of this intriguing phenomenon remain shrouded in mystery. Evolution and extinction over hundreds of millions of years have blurred the details of the transition, and the answers provided by genome sequencing only lead to more questions.

“New studies are always pushing the envelope on our thinking,” says evolutionary biologist Mansi Srivastava of the Whitehead Institute for Biomedical Research in Massachusetts. Since scientists began studying a much wider array of animals, far afield from the classic model systems of fruit flies and mice, “our thinking about what having certain kinds of genes means to being an animal has shifted.”

“These genes that we previously thought were associated with complex multicellular animals really have to do with basic multicellular functions—to get the simplest multicellular animals, you have to have these genes present,” says Srivastava, who coauthored the analysis.

As some of the most ancient animals, sponges can provide information regarding the evolution of the metazoan lineage, but for true insights about the origin of multicellularity, scientists must look even further back on the evolutionary tree. Choanoflagellates, unicellular organisms that look remarkably similar to the feeding structures of sponges, are the closest living relatives of metazoans. It turns out that they also share a number of genes once thought to be unique to multicellular animals. Tyrosine kinases (TK), for example, enzymes that function in cell-cell interactions and regulation of development in animals, were identified in the choanoflagellates in the early part of this decade, and the first sequenced choanoflagellate genome, published in 2008, revealed that they have more TK genes than any animal—and many other components of the TK signaling pathway as well.

“So this gene family that was thought to be essentially a trigger that unleashed animal origins, we can now say with great confidence evolved long before the origin of animals,” says evolutionary biologist Nicole King of the University of California, Berkeley, who has been studying choanoflagellate biology for over 10 years.

Scientists have also identified choanoflagellate homologs of cadherins, known to be involved in cell-cell adhesion and signaling in animals. And more recently, a widespread search for genes associated with integrin-mediated adhesion and signaling pathways revealed that the integrin adhesion complex originated much earlier than even the choanoflagellates, dating back to the common ancestor of animals and fungi. 3

“It’s pretty surprising to find these adhesion genes in far-flung species,” says Srivastava. “We would have thought that integrin signaling has to do with cells sticking together, but it goes much further back in time than our most recent unicellular cousins.”

The genomic exploration of the evolution of multicellularity is really just beginning, but already, a trend is emerging. “Almost every month now we are seeing genes that were supposed to be exclusive to metazoans that are already present in their single-cell relatives,” says evolutionary biologist Iñaki Ruiz-Trillo of the University of Barcelona. “I think that means co-option of ancestral genes into new functions is important for evolutionary innovations like the origin of multicellularity.”

“Probably the more data we collect, the fewer and fewer animal-specific genes there are going to be,” agrees Dunn. “And we’re going to have to explain the origins of multicellularity in terms of changes in the way these gene products interact with each other.”

“What we’d really like to be able to do is compare signaling pathways overall and see how they evolved,” Miller says. “We know a lot about the proteins themselves, but it would be great to have a glimpse into a simple pathway where we can begin to unravel what the core elements of the pathway are before layers and layers of additional regulatory elements were added, as we see in metazoan cells.”Unfortunately, because the genomics data are so new, experimental data regarding the functions of these genes in single-celled organisms remains limited. Research by biochemist Todd Miller of Stony Brook University in New York and his colleagues, for example, demonstrated that while tyrosine kinases exist in great numbers in choanoflagellates, they lack the tight regulation found in animal signaling pathways, suggesting regulatory elements may have been key to the evolution of multicellularity. But this idea remains speculative, Miller says, as the targets of these enzymes in the unicellular relatives of animals and the details of their activation are still unknown.

To confuse matters more, the vast stretches of time that separate most multicellular organisms from their unicellular cousins—more than half a billion years, in most cases—make for a lot of uncertainty. And as sequencing studies raise more questions, phylogenetic studies are also throwing a shadow of doubt on the animal tree. For example, are sponges really the most basal animals, as has long been thought? A recent phylogenetic study performed by Dunn and his colleagues suggested that perhaps ctenophores (comb jellies) are the earliest diverging extant multicellular animals. 4 “Either sponges or ctenophores are sister to all other animals,” Dunn says. “The answer you get depends still on the organisms you include in the analysis, the analysis methods you use, and what genes you look at.”

“In order to understand evolutionary transitions, you need to have a robust phylogenetic framework,” says Ruiz-Trillo. The more genomes are sequenced, the better the phylogenies get, and the more similarities and differences are recognized between multicellular organisms and their unicellular cousins. “It’s a really exciting time” for studying the evolution of multicellularity, King says. With so many open questions and more and more sequenced genomes available each year, “there’s a lot of low-hanging fruit.”

A multicellular model?

Animals aren’t the only multicellular organisms, of course, and thus not the only system applicable to the study of multicellularity’s origins. In fact, multicellularity is believed to have evolved as many as 25 different times among living species. So while the search for metazoan origins may be riddled with uncertainty, perhaps scientists can draw inferences from the study of multicellularity in other lineages.

Comparing brown algae to their unicellular diatom relatives, for example, researchers saw an increase in membrane-spanning receptor kinases, a protein family known to play a role in cellular differentiation and patterning in both animals and green plants.[url= 5][/url]5 The independent evolution of more kinase genes in each of these lineages suggests that this family of proteins may have been key to this transition.

Of all the multicellular lineages, however, the volvocine green algae represent the best-studied and most tractable system for teasing out the evolution of multicellularity. In contrast to most other origins of multicellularity, which likely arose close to a billion years ago, the change to multicellularity in these algae may have occurred as little as 200 million years ago—possibly limiting evolution’s mark on their genomes. Furthermore, between the unicellular Chlamydomonas species and the most-derived multicellular Volvoxthere are several extant intermediate species, some of which appear to have changed little since their divergence from their unicellular ancestors. While recent evidence indicates a complicated evolutionary history, including multiple origins of some traits and reversals,[url= 6][/url]6 this lineage nonetheless presents a phylogenetic road map by which step-by-step transitions can be inferred. (See illustration)

Volvocine algae are aquatic, flagellated eukaryotes that range in complexity from unicellular species to a variety of colonial forms to multicellular Volvox, some of which boast up to 50,000 cells. This transition involved a series of key innovations, including cell-cell adhesion, inversion, and differentiation of somatic and germ cell lines. Two species, in particular, have become models for the evolution of multicellularity—the single-celled Chlamydomonas reinhardtii and the 2,000-or-so-celled Volvox carteri.

As with animals, comparisons of their recently sequenced genomes have revealed that there are few striking differences among the genetic codes of these organisms that could explain the drastic differences in their morphology. “It was pretty disappointing at first,” admits developmental biologist Stephen Miller of the University of Maryland, Baltimore County, who helped to analyze the Volvox genome (the sequence was published last summer). “We were hoping to see differences that would point to explanations for why Volvox is so much more developmentally complex than Chlamydomonas, but that certainly wasn’t the case.”

Not only do the genes exist in Chlamydomonas, they are so similar to the Volvox versions that they appear to be able to stand in for missing or mutant copies in their multicellular cousins. Volvox’s glsA gene, for example, codes for an essential component of asymmetric division; glsA mutants can only divide symmetrically, resulting in adults comprised entirely of small somatic cells, with none of the large germ cells, known as gonidia, that normally give rise to the next generation. While the homologous protein in Chlamydomonas is only about 70 percent identical to glsA’s protein, it can restore asymmetric cell division when the gene is transformed into glsA mutants. “Its ortholog in Chlamydomonas is perfectly capable of carrying out the same function,” Miller says.

Similarly, invA is essential to the process known as inversion, which gives adult Volvox their spherical shape, with the gonidia on the inside and the small, flagellated somatic cells around the exterior. In invAmutants, inversion fails to occur due to the cells’ inability to move relative to the cytoplasmic bridges that connect them, and the gonidia are exposed on the surface of the spheroid. Just like glsA mutants, however, this phenotype can be rescued by the transformation of the Chlamydomonas ortholog, known asIAR1.

There are exceptions to this pattern, however, such as the appearance in Volvox of many new genes that encode cell wall or extracellular matrix (ECM) proteins, with a dramatic increase in the number and variety of Volvox genes in two major ECM protein families, as compared with Chlamydomonas. While Volvox carteri have only a couple thousand times as many cells as Chlamydomonas, they can grow to more than 100,000 times larger thanks to a dramatic increase in the amount of ECM, which constitutes more than 99 percent of the volume of a mature Volvox.

Another significant genetic change in Volvox becomes evident when examining the mating locus—a region on one chromosome containing sex-specific genes that dictate whether the organism will be male or female during the sexual part of the volvocine life cycle. A notable difference in the sexual strategies of Chlamydomonas and Volvox is the size of their gametes. While the sperm and the egg of Chlamydomonasare nearly indistinguishable and are produced in similar quantities, Volvox eggs are significantly larger than its sperm, and there are far fewer of them. This transition to oogamy, as it’s called, appears to be a hallmark of multicellularity.

“It’s a remarkably conserved trait,” says cell and evolutionary biologist James Umen of The Salk Institute. “When you look at any lineage that becomes multicellular and has sex, it almost invariably goes from having mating types where the gametes are same size to having a sperm/egg system of some sort.” And in contrast to most of the innovations associated with the asexual reproductive phase of the Volvox life cycle, new genes do seem to be a big part of the evolution of dimorphic gametes. The mating locus of Volvox is greatly expanded to more than 500 percent of the size of Chlamydomonas’ 200–300 kilobase mating locus, and contains many genes that fall outside the mating locus in Chlamydomonas, as well as at least 13 new gender-specific genes. 7

Volvox kind of exploded in terms of size and context,” says Umen. “In general, things related to sex don’t follow the normal rules regarding evolution; innovation seems to be a really important part of sex.”

Why not admit evolution is simply not a feasible explanation for the rise of sex? 

But how much can scientists learn about the evolution of the complex multicellularity exhibited by animals and other lineages from studying the volvocine algae? According to some, not much. Volvox represents a relatively simple form of multicellularity, with only two cell types and no organized tissues or organs.

“I think it’s dangerous to generalize too much,” says Stephen Miller. “Because [multicellularity] has evolved independently in each of these cases, there don’t have to be similarities in how it evolved. But I would guess there might end up being some common themes.”

The switch from single-celled organisms to ones made up of many cells have supposedly evolved independently more than two dozen times.  If evolution and transition from unicellular to multicellular life is exceedingly complex, the chance that it happened once is also exceedingly small. That it happened multiple times separately, becomes even more remotely possible. Convergent evolution of similar traits is evidence against, not for evolution. In order to infer that a proposition is true, these nuances are important to observe. The key is in the details. As Behe states: In order to say that some function is understood, every relevant step in the process must be elucidated. The relevant steps in biological processes occur ultimately at the molecular level, so a satisfactory explanation of a biological phenomenon such as the de novo make of cell communication and cell junction proteins essential for multicellular life must include a molecular explanation.

One emerging idea is that complex multicellularity, such as that of animals, plants, and fungi, may have evolved only a handful of times, and that it almost always resulted from the division of a single cell into the components of the larger organism, King says. In contrast to slime molds, for example, which form via aggregation of neighboring cells, the earliest multicellular animals were likely to have evolved by failing to disperse after the mother cell divided.

The cells had not only to hold together, but important mechanisms to stick the cells together had to emerge, that is, the ability of individual cells to associate in precise patterns to form tissues, organs, and organ systems requires that individual cells be able to recognize, adhere to, and communicate with each other. Thus, the apparatus of cell junctions and the extracellular matrix is critical for every aspect of the organization, function, and dynamics of multicellular structures. The arise of adhesive junctions, tight junctions and gap junctions,  and how they emerged is, therefore, a key factor to explain multi-cellular life. The cells of multi-cellular organisms detect and respond to countless internal and extracellular signals that control their growth, division, and differentiation during development, as well as their behavior in adult tissues. At the heart of all these communication systems are regulatory proteins that produce chemical signals, which are sent from one place to another in the body or within a cell, usually being processed along the way and integrated with other signals to provide clear and effective communication. The rise of these communication channels had to arise together with junction mechanisms in order to establish successful multicellular organisms. One feature without the other would not have provided success and advantage of survival. This is an important, essential and fundamental macroevolutionary change, and the explanation of macro-evolution must account for these changes, and provide feasible possible and likely ways of evolution. Beside this,  a shift on several levels of biological organization had to occur, providing a considerable advantage of survival, considering that for example  one of the first cooperative steps required for the evolution of multicellularity in the volvocine algae was the development of the extracellular cell matrix from cell wall components, which can be metabolically costly to produce. But much more is required. Ann Gauger: New genes and proteins must be invented. The cytoskeleton, Hox genes, desmosomes, cell adhesion molecules, growth factors, microtubules, microfilaments, neurotransmitters, whatever it takes to get cells to stick together, form different shapes, specialize, and communicate must all come from somewhere. Regulatory proteins and RNAs must be made to control the expression in time and space of these new proteins so that they all work together with existing pathways.In fact, in order for development to proceed in any organism, a whole cascade of coordinated genetic and biochemical events is necessary so that cells divide, change shape, migrate, and finally differentiate into many cell types, all in the right sequence at the right time and place. These cascades and the resulting cell divisions, shape changes, etc., are mutually interdependent. Interrupting one disrupts the others. 9

Perhaps the evolution of advanced multicellularity wasn’t so easy after all. “There are lots and lots of transitions from single cells to organisms that have more than one cell, but there are a lot fewer transitions that go as far as evolving into complex multicellular organisms with cellular differentiation,” Herron says. “That only happened a handful of times.”

Or maybe it never happened, because its not possible by natural means, without a creative power involved....

Evidence of this comes from a recent study out of King’s lab that found choanoflagellates fail to form colonies when cell division is inhibited. If the earliest ancestors of animals were anything like modern-day choanoflagellates, this suggests that animal development from a single-celled embryo is core to our evolution, and not a secondary development.

Similarly, the volvocine algae all divide via multiple fission, where the nucleus divides many times before the cytoplasm splits to generate that number of daughter cells. “It’s a way of producing a large number of genetically identical cells all at once,” says evolutionary biologist Matthew Herron of the University of British Columbia. “The only thing you need to do to produce an eight-cell colony [is have] them to stick together.”

Complexity breeds cooperation

The collaboration of first a few, then millions of cells to create an entirely new kind of “individual” thus requires a shift in the level of biological organization upon which natural selection acts. In this way, the evolution of multicellularity can be considered what has been termed an “evolutionary transition in individuality” (ETI), where the unit of selection changes from a single cell to a group of cells—the newly evolved multicellular individual. Other ETIs include the congregation of replicating molecules to yield the first prokaryotic cells, the associations of prokaryotic cells to create eukaryotic cells with organelles such as chloroplasts and mitochondria, and the establishment of cooperative societies composed of discrete multicellular individuals, like eusocial insect colonies.Beyond the molecular and developmental logistics of evolving multicellularity, there is the added complication of genetic conflict. An incredible amount of cooperation is required for individual cells to come together and function as one, and with natural selection acting at the level of the individual cell, there will be significant evolutionary pressure to cheat the system and sabotage the success of the multicellular whole.

“The general principle is, in any of these kinds of transitions there’s always some form of cooperation that’s needed,” says Herron. “In the example of the ants and bees, it’s the workers that are being cooperative in the sense that they’re sacrificing their own reproduction in order to help the queen reproduce. And in multicellular organisms like us and Volvox, the somatic cells are cooperating in the sense that they’re sacrificing their own reproduction in order to help the reproductive cells reproduce.”

But such transitions are not always smooth, as conflict can arise when selfish mutations result in cheaters that attempt to benefit from the group without contributing their fair share. One of the first cooperative steps required for the evolution of multicellularity in the volvocine algae was the development of the ECM from cell wall components, which can be metabolically costly to produce. The ECM can thus be thought of as a shared resource, and cells that do not contribute to its production may still benefit from its existence, thus gaining a growth or reproductive advantage.

CreatureCast - Multicellularity from Casey Dunn on Vimeo.

To defend themselves against such cheating, these new kinds of individuals must evolve mechanisms of conflict mediation. One proposed theory for how the volovcine algae defend themselves against ECM cheaters is the evolution of genetic control of cell number. In unicellular Chlamydomonas, the number of cells produced depends on the size of the parent cell, which in turn is contingent on the amount of resources available. Under these circumstances, it is conceivable that a cell in a multicellular organism could benefit from not contributing to ECM production by putting that saved energy to use making more offspring cells. But all volvocine algae that have evolved an ECM have also switched to genetic control over cell number. As a result, cheaters have less to gain because the total number of daughter cells produced by the group is limited.

The somatic regenerator, or regA, gene appears to be one important factor in keeping somatic cells from defecting. In regA mutants, somatic cells develop normally at first, but then they enlarge and develop into gonidia that can divide to yieldVolvox offspring. “What it causes is a dysfunctional colony,” Herron says. “In the lab, we can keep these mutant colonies alive, but they sink to the bottom of the test tube. We assume that they would not last long in nature.”The differentiation of somatic and germ cells to yield a division of labor between viability and reproduction represents another potential conflict. In essence, somatic cells are giving up their own reproductive output to support the success of the entire colony of cells, presumably by providing enhanced motility. They don’t always cooperate willingly, however, Herron says; mutations still arise that cause some somatic cells in Volvox to try to reproduce on their own rather than support the entire organism’s reproductive success as sterile swimmers.

One proposed mechanism of conflict mediation following this transition is the early segregation of the germ line. The Volvox gonidia that will produce the next generation are formed by just a few rounds of asymmetric cell division very early in development, so there is little time for mutations to accumulate in these cells. While somatic cells may still accumulate mutations, these defects will not be passed on. “They are evolutionary dead ends,” Herron says.

These recurrent mutations in Volvox suggest that “the conflict between the individual cells and the interest of colony may still be going on,” he adds. Such conflict may limit the organism’s complexity, as selection on individual cells battles with the whole organism’s attempt to survive and reproduce, suggesting that perhaps the evolution of advanced multicellularity wasn’t so easy after all. “There are lots and lots of transitions from single cells to organisms that have more than one cell, but there are a lot fewer transitions that go as far as evolving into complex multicellular organisms with cellular differentiation,” Herron says. “That only happened a handful of times.”


  1. M. Srivastava et al., “The Amphimedon queenslandica genome and the evolution of animal complexity,” Nature, 466:720-26, 2010. Free F1000 Evaluation
  2. N. King et al., “The genome of the choanoflagellate Monosiga brevicollis and the origin of metazoans,” Nature, 451:783-88, 2008. Free F1000 Evaluation
  3. A. Sebé-Pedrós et al., “Ancient origin of the integrin-mediated adhesion and signaling machinery,” PNAS, 107:10142-47, 2010.
  4. C.W. Dunn et al., “Broad phylogenomic sampling improves resolution of the animal tree of life,”Nature, 452:745-49, 2008. Free F1000 Evaluation
  5. J.M. Cock et al., “The Ectocarpus genome and the independent evolution of multicellularity in brown algae,” Nature, 465:617-21, 2010. Free F1000 Evaluation
  6. M.D. Herron et al., “Triassic origin and early radiation of multicellular volvocine algae,”PNAS,106:3254-58. 2009.
  7. P. Ferris et al., “Evolution of an expanded sex-determining locus in Volvox,” Science, 328:351-54, 2010.
  8. S.R. Fairclough et al., “Multicellular development in a choanoflagellate,” Current Biology, 20:R875-76, 2010.


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A Simple Transition to Multicellularity -- Not! 1

Volvox is a small spheroid green alga that lives in ponds, making its living by photosynthesis as plants do. Volvox is among the simplest animals to have more than one cell type. The hollow sphere that is its body is made up of somatic cells (soma is the Greek word for body). Within the sphere are specialized cells called gonidia (from the Greek gonē, meaning generation or seed). Early in embryogenesis, some cells divide to produce large cells. These become the gonidia, which then become embryos with their own seeds of gonidia. Eventually the embryos mature into the next generation of Volvox, with their own embryos growing inside. Interestingly, though, when times get hard and the pond starts to dry up or things get too hot, the embryos develop into female and male forms that produce eggs and sperm rather than divide asexually. These eggs and sperm fuse to make new diploid Volvox, which then goes into a sort of stasis until the water returns. That's a neat trick. Then the asexual cycle starts all over again. Volvox somatic cells each have two flagella. The whip-like flagella help these little spheroid creatures to swim in a sort of gentle ballet. See here:

The somatic cells are embedded in an extracellular matrix, a gel-like substance that supports and surrounds the cells. The somatic cells in the video appear as an outer green haze on the spinning spheres. The bright green small spheres within the bodies of the Volvox are the developing embryos. Volvox is often used as an example of how the evolution to multicellularity might have happened. The story is that single flagellate cells like C. reinhardtii(which I wrote about here earlier this week) first bundled together, then the bundled cells took on a more organized shape, perhaps to aid swimming, then those groups developed several cell types that could divide the labor among themselves. The beginning of more complex life forms, perhaps?

To hear the story told, it seems a simple progression. Only one or two or genes might be necessary to get the cells to form clumps by incomplete cell divisions. There are species that look like this stage -- clumps of cells that swim and then stop swimming and divide. How those cells separate is another question. A few more hypothetical genes would be necessary to make the extracellular matrix in which most species embed their cells and then to digest it when the right time comes. Then the final essential step is taken, the division of labor between somatic and reproductive cells. Some cells grow into little embryos and then adults, while other cells adopt a supportive role, contributing food to the growing embryos inside. A theory has been proposed involving 12 steps for how this change from single-celled to multicellular Volvox might have happened.

Missing from this story, though, are the details necessary for this 12-step progression to occur. There's the matter of incomplete cell division, cell separation later, and matrix formation. Then there's the matter of specialization. To get the specialization of somatic from germ cells requires the development of at least three proteins. Also, the embryos produced by those reproductive cells are inside out -- the flagella are on the inside, which makes them useless for swimming, and the gonidia are on the outside. As a result, the embryo must turn itself inside out when it reaches the right size. This requires that the somatic cells change shape to bottle- or spindle-shaped cells, depending on their position in the embryo. This shape change requires both microtubules and a little motor protein called kinesin. Neither microtubules or kinesin are present in bacteria so their origin must be accounted for. The selective advantage of each step is not clear.
Later, the parent Volvox produces an enzyme that digests the matrix the somatic cells are embedded in, and releases the embryos. The somatic cells commit suicide by a process known as apoptosis -- programmed cell death --that I wrote about here. This process involves a minimum of several novel genes as well.

Finally, there is the not so small matter of sexual reproduction. Getting two kinds of reproductive cells, eggs and sperm, requires triggering a new set of regulatory genes to change the pattern of gene expression, so as to produce the two cell types. And more than that -- going into stasis, recovering from stasis, and going from diploid to haploid again requires yet more regulation. (Volvoxnormally has only one set of chromosomes -- they are haploid -- but after fusion of egg and sperm they are diploid -- having two sets of chromosomes.)
Does the story seem simple now? When you think of it as just incomplete divisions and a three-gene regulatory scheme coopted from other jobs to cause the switch from somatic to reproductive cells, it sounds plausible. When you add the other requirements, though, the story becomes untenable. A coordinated process like inversion requires specific cell shape changes signaled by some process, and requiring microtubules and kinesin at a minimum. (Both of these proteins are necessary for multiple other cellular processes, by the way, but are new to eukaryotes.) And remember, inversion is a necessary process -- without it the embryos can't swim. Next the digestive enzyme must be produced at the right time, which no doubt involves some signaling process, and all the (new) proteins involved in programmed cell death (also new to eukaryotes) must be made and/or activated.

Where do all these new proteins come from? Either they come from cooption of old proteins, or by making new ones. I've already been over how hard those processes are to accomplish multiple times. Where does their regulation come from? That involves yet more proteins to serve as genetic switches, which also must be coopted or made from spare sequence lying around. It's an infinite regress of steps to be filled, and answering one question about mechanism leads to many more. I think asking these questions is well worth the effort. With each answer found we learn something more about the way things work in living things, and we find similarities and differences and discern underlying principles. But what I object to is the evolutionary gloss put on these similarities and differences, these principles. It's one thing to say things were coopted from some unknown precursor protein, and another to demonstrate that such cooption is possible. This is the sort of detail that requires answering if the white space in evolutionary thinking is to be filled. Saying that something might have happened is not the same as showing that it actually could happen.


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Multicellularity: The Evolution of Differentiation 1

One of evolution's most important experiments was the creation of multicellular organisms. There appear to be several paths by which single cells evolved multicellular arrangements; . The first path involves the
orderly division of the reproductive cell and the subsequent differentiation of its progeny into different cell types. This path to multicellularity can be seen in a remarkable series of multicellular organisms collectively referred to as the family Volvocaceae, or the volvocaceans (Kirk 1999).

The Volvocaceans

The simpler organisms among the volvocaceans are ordered assemblies of numerous cells, each resembling the unicellular protist Chlamydomonas, to which they are related (Figure A).

A single organism of the volvocacean genus Gonium (Figure B), for example, consists of a flat plate of 4 to 16 cells, each with its own flagellum. In a related genus, Pandorina, the 16 cells form a sphere (Figure C); and in Eudorina, the sphere contains 32 or 64 cells arranged in a regular pattern (Figure D). In these organisms, then, a very important developmental principle has been worked out: the ordered division of one cell to generate a
number of cells that are organized in a predictable fashion. As occurs during cleavage in most animal embryos, the cell divisions by which a single volvocacean cell produces an organism of 4 to 64 cells occur in very rapid sequence and in the absence of cell growth.

The next two genera of the volvocacean series exhibit another important principle of development: the differentiation of cell types within an individual organism. The reproductive cells become differentiated from the somatic cells. In all the genera mentioned earlier, every cell can, and normally does, produce a complete new organism by mitosis. In the genera Pleodorina and Volvox, however, relatively few cells can reproduce. In Pleodorina californica (Figure E), the cells in the anterior region are restricted to a somatic function; only those cells on the posterior side can reproduce. In P. californica, a colony usually has 128 or 64 cells, and the ratio of the number of somatic cells to the number of reproductive cells is usually 3:5. Thus, a 128-cell colony typically has 48 somatic cells, and a 64-cell colony has 24.

In Volvox, almost all the cells are somatic, and very few of the cells are able to produce new individuals. In some species of Volvox, reproductive cells, as in Pleodorina, are derived from cells that originally look and function like somatic cells before they enlarge and divide to form new progeny. However, in other members of the genus, such as V. carteri, there is a complete division of labor: the reproductive cells that will create the next generation are set aside during the division of the original cell that is forming a new individual. The reproductive cells never develop functional flagella and never contribute to motility or other somatic functions of the
individual; they are entirely specialized for reproduction. Thus, although the simpler volvocaceans may be thought of as colonial organisms (because each cell is capable of independent existence and of perpetuating the species), in V. carteri we have a truly multicellular organism with two distinct and interdependent cell types (somatic and reproductive), both of which are required for perpetuation of the species (Figure F). Although not all animals set aside the reproductive cells from the somatic cells (and plants hardly ever do), this separation of germ cells from somatic cells early in development is characteristic of many animal phyla

Although all the volvocaceans, like their unicellular relative Chlamydomonas, reproduce predominantly by asexual means, they are also capable of sexual reproduction, which involves the production and fusion of haploid gametes. In many species of Chlamydomonas, sexual reproduction is isogamous ("the same gametes"), since the haploid gametes that meet are similar in size, structure, and motility. However, in other species of Chlamydomonas as well as many species of colonial volvocaceans swimming gametes of very different sizes are produced by the different mating types. This pattern is called heterogamy ("different gametes"). But the larger volvocaceans have evolved a specialized form of heterogamy, called oogamy, which involves the production of large, relatively immotile eggs by one mating type and small, motile sperm by the other (see Sidelights and Speculations). Here we see one type of gamete specialized for the retention of nutritional and developmental resources and the other type of gamete specialized for the transport of nuclei. Thus, the volvocaceans include the simplest organisms that have distinguishable male and female members of the species and that have distinct developmental pathways for the production of eggs or sperm. In all the volvocaceans, the fertilization reaction resembles that of Chlamydomonas in that it results in the production of a dormant diploid zygote, which is capable of surviving harsh environmental conditions. When conditions allow the zygote to germinate, it first undergoes meiosis to produce haploid offspring of the two different mating types in equal numbers.

Differentiation and Morphogenesis in Dictyostelium: Cell Adhesion

The life cycle of dictyostelium

Another type of multicellular organization derived from unicellular organisms is found in Dictyostelium discoideum.* The life cycle of this fascinating organism is illustrated below

In its asexual cycle, solitary haploid amoebae (called myxamoebae or "social amoebae" to distinguish them from amoeba species that always remain solitary) live on decaying logs, eating bacteria and reproducing by binary fission. When they have exhausted their food supply, tens of thousands of these myxamoebae join together to form moving streams of cells that converge at a central point. Here they pile atop one another to produce a conical mound called a tight aggregate. Subsequently, a tip arises at the top of this mound, and the tight aggregate bends over to produce the migrating slug (with the tip at the front). The slug (often given the more dignified title of pseudoplasmodium or grex) is usually 2 4 mm long and is encased in a slimy sheath. The grex begins to migrate (if the environment is dark and moist) with its anterior tip slightly raised. When it reaches an illuminated area, migration ceases, and the grex differentiates into a fruiting body composed of spore cells and a stalk. The anterior cells, representing 15 20% of the entire cellular population, form the tubed stalk. This process begins as some of the central anterior cells, the prestalk cells, begin secreting an extracellular coat and extending a tube through the grex. As the prestalk cells differentiate, they form vacuoles and enlarge, lifting up the mass of prespore cells that had made up the posterior four-fifths of the grex (Jermyn and Williams 1991). The stalk cells die, but the prespore cells, elevated above the stalk, become spore cells. These spore cells disperse, each one becoming a new myxamoeba. In addition to this asexual cycle, there is a possibility for sex in Dictyostelium. Two myxamoebae can fuse to create a giant cell, which digests all the other cells of the aggregate. When it has eaten all its neighbors, it encysts itself in a thick wall and undergoes meiotic and mitotic divisions; eventually, new myxamoebae are liberated. Dictyostelium has been a wonderful experimental organism for developmental biologists because initially identical cells are differentiated into one of two alternative cell types, spore and stalk. It is also an organism wherein individual cells come together to form a cohesive structure composed of differentiated cell types, akin to tissue formation in more complex organisms. The aggregation of thousands of myxamoebae into a single organism is an incredible feat of organization that invites experimentation to answer questions about the mechanisms involved.

Cell adhesion molecules in dictyostelium

How do individual cells stick together to form a cohesive organism? This problem is the same one that embryonic cells face, and the solution that evolved in the protists is the same one used by embryos: developmentally regulated cell adhesion molecules

While growing mitotically on bacteria, Dictyostelium cells do not adhere to one another. However, once cell division stops, the cells become increasingly adhesive, reaching a plateau of maximum cohesiveness around 8 hours after starvation. The initial cell-cell adhesion is mediated by a 24,000-Da (24-kDa) glycoprotein that is absent in myxamoebae but appears shortly after division ceases (Knecht et al. 1987; Loomis 1988). This protein is synthesized from newly transcribed mRNA and becomes localized in the cell membranes of the myxamoebae. If myxamoebae are treated with antibodies that bind to and mask this protein, they will not stick to one another, and all subsequent development ceases.

Once this initial aggregation has occurred, it is stabilized by a second cell adhesion molecule. This 80-kDa glycoprotein is also synthesized during the aggregation phase. If it is defective or absent in the cells, small slugs will form, and their fruiting bodies will be only about one-third the normal size. Thus, the second cell adhesion system seems to be needed for retaining a large enough number of cells to form large fruiting bodies (Müller and Gerisch 1978; Loomis 1988). In addition, a third cell adhesion system is activated late in development, while the slug is migrating. This protein appears to be important in the movement of the prestalk cells to the apex of the mound (Ginger et al. 1998). Thus, Dictyostelium has evolved three developmentally regulated systems of cell-cell adhesion that are necessary for the morphogenesis of individual cells into a coherent organism. As we will see , metazoan cells also use cell adhesion molecules to form the tissues and organs of the embryo.

Dictyostelium is a "part-time multicellular organism" that does not form many cell types (Kay et al. 1989), and the more complex multicellular organisms do not form by the aggregation of formerly independent cells. Nevertheless, many of the principles of development demonstrated by this "simple" organism also appear in embryos of more complex phyla (see Loomis and Insall 1999). The ability of individual cells to sense a chemical gradient (as in the myxamoeba's response to cAMP) is very important for cell migration and morphogenesis during animal development. Moreover, the role of cell surface proteins in cell cohesiveness is seen throughout the animal kingdom, and differentiation-inducing molecules are beginning to be isolated in metazoan organisms.

Differentiation in dictyostelium

Differentiation into stalk cell or spore cell reflects another major phenomenon of embryogenesis: the cell's selection of a developmental pathway. Cells often select a particular developmental fate when alternatives are available. A particular cell in a vertebrate embryo, for instance, can become either an epidermal skin cell or a neuron. In Dictyostelium, we see a simple dichotomous decision, because only two cell types are possible. How is it that a given cell becomes a stalk cell or a spore cell? Although the details are not fully known, a cell's fate appears to be regulated by certain diffusible molecules. The two major candidates are differentiationinducing factor (DIF) and cAMP. DIF appears to be necessary for stalk cell differentiation. This factor, like the sex-inducing factor of Volvox, is effective at very low concentrations (10-10M); and, like the Volvox protein, it appears to induce differentiation into a particular type of cell. When added to isolated myxamoebae or even to prespore (posterior) cells, it causes them to form stalk cells. The synthesis of this low molecular weight lipid is genetically regulated, for there are mutant strains of Dictyostelium that form only spore precursors and no stalk cells. When DIF is added to these mutant cultures, stalk cells are able to differentiate (Kay and Jermyn 1983; Morris et al. 1987), and new prestalk-specific mRNAs are seen in the cell cytoplasm (Williams et al. 1987). While the mechanisms by which DIF induces 20% of the grex cells to become stalk tissue are still controversial (see Early et al. 1995), DIF may act by releasing calcium ions from intracellular compartments within the cell (Shaulsky and Loomis 1995).

Although DIF stimulates myxamoebae to become prestalk cells, the differentiation of prespore cells is most likely controlled by the continuing pulses of cAMP. High concentrations of cAMP initiate the expression of presporespecific mRNAs in aggregated myxamoebae. Moreover, when slugs are placed in a medium containing an enzyme that destroys extracellular cAMP, the prespore cells lose their differentiated characteristics (Figure 2.20; Schaap and van Driel 1985; Wang et al. 1988a,b).

1) Development biology, Scott F. Gilbert pg.29

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Multicellularity has evolved supposedly at least once in every major eukaryotic clade ( branch ) (in all ploidy levels) and numerous times among the prokaryotes. According to a standard multilevel selection (MLS) model, in each case, the evolution of multicellularity required the acquisition of cell–cell adhesion, communication, cooperation, and specialization attended by a compulsory alignment-of-fitness phase and an export-of-fitness phase to eliminate cell–cell conflict and to establish a reproductively integrated phenotype. These achievements are reviewed in terms of generalized evolutionary developmental motifs (or “modules”) whose overall logic constructs were mobilized and executed differently in bacteria, plants, fungi, and animals. When mapped onto a matrix of theoretically possible body plan morphologies (i.e., a morphospace), these motifs and the MLS model identify a “unicellular Ÿ colonial Ÿ multicellular” transformation series of body plans that mirrors trends observed in the majority of algae (i.e., a polyphyletic collection of photoautotrophic eukaryotes) and in the land plants, fungi, and animals. However, an alternative, more direct route to multicellularity theoretically exists, which may account for some aspects of fungal and algal evolution, i.e., a “siphonous Ÿ multicellular” transformation series. This review of multicellularity attempts to show that natural selection typically acts on functional traits rather than on the mechanisms that generate them (“Many roads lead to Rome.”) and that genome sequence homologies do not invariably translate into morphological homologies (“Rome isn’t what it used to be.”).

This paper reviews the evolutionary origins of multicellularity and explores the developmental bio -logic constructs required for the fabrication of a multicellular body plan. A broad
comparative approach is adopted because multicellularity has evolved multiple times in different ways in very different clades ( Fig. 1 )

and because different criteria have been established to define individuality in the context of multicellularity ( Herron et al., 2013 ). Estimates of the exact number of times vary, depending on how multicellularity is defined and in what phylogenetic context. When described simply as a cellular aggregation, multicellular organisms are estimated conservatively to have evolved in at least 25 lineages , making it a “minor major” evolutionary transformation. When more stringent criteria are applied, as for example a requirement for sustained cell-to-cell interconnection, communication, and cooperation, multicellularity has evolved multiple times in bacteria (e.g., Actinobacteria, Myxobacteria, and Cyanobacteria; , but only once in the Animalia, three times in the Fungi (chytrids, ascomycetes, and basidiomycetes), and six times among the algae (twice each in the rhodophytes, stramenopiles, and chlorobionta; . Regardless of a canonical definition or an exact count of its occurrence on the tree of life, the emergence of multicellularity raises a number of important but as yet unresolved questions. For example, what if any are the selection barriers to (and the drivers toward) it? Are the motifs in the morphological transformation series that are seen in multicellular lineages the result of adaptive evolution, relaxed selection, or the inevitable consequences of generic physical laws coupled to very simple genomic processes? Is there a genomic toolkit or a set of “master genes” responsible for multicellularity, and are they shared among all eukaryotic clades? Indeed, are the multiple origins of multicellularity truly independent, given that all eukaryotes ultimately shared a last common ancestor? This last question is particularly intriguing in light of (1) multilevel selection theory that requires the evolution of an alignment-of-fi tness among the cells of a multicellular progenitor and (2) the fact that all eukaryotes shared a last common unicellular ancestor that must have evolved an alignment among the various metabolic interests of its endosymbionts to integrate the activities of its protoorganelles, e.g., the TOC–TIC translocon protein-import system of the land-plant plastid envelope incorporates a cyanobacterialike core .

Many workers have addressed these and other questions, often in very different ways that refl ect their taxonomic or research focus . The perspective taken in this review is an evolutionary-developmental perspective, which shows that a phenotypic novelty can be achieved by the acquisition of similar developmental motifs or “modules” that nevertheless differ in how they are mobilized or executed in different kinds of organisms. Consider the criteria for sustained cell–cell adhesion and communication in the construction of a multicellular organism. Intercellular adhesion in the brown algae involves phlorotannins and polymers of D -mannuronic and L -guluronic acids ; among the land plants  (embryophytes), it is achieved by a middle lamella typically dominated by Ca 2+ -rhamnogalacturonanic-rich pectins, produced by many fungi. Likewise, intercellular communication in the embryophytes involves plasmodesmata , which differ significantly from the desmosomes and the tight or gap junctions of chordates ( Fig. below )

the plasmodesmata-like structures seen in some brown algae, or the cytoplasmic bridges in Volvox and colonial choanofl agellates . Nevertheless, it is very likely that cell–cell adhesives and intercellular communication modules evolved from the co-option of mechanisms participating in the life cycles of unicellular ancestral life-forms . For example, molecular analyses identify a diversity of cadherins in the unicellular choanoflagellate Monosiga brevicollis (an early-divergent taxon from the unicellular metazoan progenitor) that appear to function in environment-responsive, intracellular signal transduction, e.g., tyrosine kinase and hedgehog signaling . By the same token, ancient intercellular communication may have evolved by the co-option of prokaryoticwhich also participate in cell wall loosening . These compounds differ chemically from the type-1 transmembrane cadherin proteins responsible for animal cell–cell adhesion or the glycoprotein-based “glues”  produced by many fungi . Likewise, intercellular communication in the embryophytes involves plasmodesmata, which differ significantly from the desmosomes and the tight or gap junctions of chordates ( Fig. above), the plasmodesmata-like structures seen in some brown algae , or the cytoplasmic bridges in Volvox and colonial choanoflagellates. Nevertheless, it is very likely that cell–cell adhesives and intercellular communication modules evolved from the co-option of mechanisms participating in the life cycles of unicellular ancestral life-forms. For example, molecular analyses identify a diversity of cadherins in the unicellular choanoflagellate Monosiga brevicollis (an early-divergent taxon from the unicellular metazoan progenitor) that appear to function in environment-responsive, intracellular signal transduction, e.g., tyrosine kinase and hedgehog signaling. By the same token, ancient intercellular communication may have evolved by the co-option of prokaryotic two-component signaling pathways involving histidine kinases, response regulators, and in some cases, histidine-containing phosphotransfer proteins  that have been identified in a broad spectrum of eukaryotes including Thalassiosira , Chlamydomonas , Dictyostelium , a variety of fungi, and Arabidopsis . Indeed, the molecular bases for cell-to-cell adhesion and communication may have evolved simultaneously in some cases, e.g., metazoan tetraspanin-enriched protein/membrane microdomains participate in cell–cell adhesion and communication as well as membrane fusion and cell migration. Much like the functionally analogous structures collectively referred to as “leaves” (but called laminae or blades by phycologists, phyllids by bryologists, and fronds by pteridologists), multicellularity is a recurrent morphological theme in evolution that was reached in different ways by different lifeforms, i.e., in cladistic parlance, multicellularity is a character with numerous character states.

The foregoing introduces two themes that will be refined throughout this review. The first is that natural selection typically acts on functional traits and not directly on their underlying generative mechanisms. This feature enables sometimes radically different variants of a developmental motif, such as cell–cell adhesion, to achieve the same functional trait. The second interrelated theme is that extensive and careful analyses are required to evaluate the hypothesis that any two developmental patterns are homologous even when they are evoked by the same molecular (genomic) sequences. This assertion also applies logically to the identification of genomic orthologies in ways that extend beyond the gene (and thus proteins or noncoding RNAs) to include the effects of domain accretion, i.e., the addition of sequences encoding extra structural domains to protein-coding genes.
These two themes are developed by

(1) presenting a brief history of evolutionary-developmental (evo-devo) biology to establish the concept of the developmental module, 
(2) reviewing and comparing the modules and their variants required to construct a multicellular organism, particularly plants, which are here broadly defined to include any eukaryotic photoautotroph (to include the polyphyletic algae), 
(3) ordering these modules in a sequence of their evolutionary occurrence that accords with a standard multilevel selection (MLS) model for multicellularity, 
(4) exploring an alternative route to multicellularity via the siphonous/coenocytic body plan, and 
(5) returning to open-ended questions such as how multistable gene expression patterns are coordinated simultaneously during the development of a multicellular life-form (by considering the genome as more than the sum of its gene expression patterns).


The role of the gene and gene networks — Beginning with a series of papers in the early 20th century and culminating with his book The Genetical Theory of Natural Selection , Ronald A. Fisher (1930) founded the field of population genetics and designated the gene as the unit of stable hereditary transmission between successive generations. This genocentric view of inheritance asserted the preeminent importance of allele frequency distributions and differential reproductive success in evolutionary processes. However, it failed to explore alternative origins of phenotypic variation. It simply assumed that all phenotypic variants result from gene mutations. Ensuing debates consequently dealt with the tempo and magnitude of mutations, but they largely ignored their causes. Perhaps even more restrictive was the additional assumption that the phenotype could be mapped directly onto the genotype and thus described simply by changes exclusively at the level of individual genes or sets of genes. This outlook was challenged in the 1970s and 1980s within a field of study soon to be called evolutionary-developmental biology, or simply evo-devo, which asserted that evolutionary phenotypic transformations are the result of changes in gene expression patterns rather than the immediate products of mutations of individual genes. Arguably perhaps, this perspective can be traced back to a seminal paper by Roy J. Britten and Eric H. Davidson entitled Gene Regulation for Higher Cells: A Theory, which focused on the connection between advances in molecular biology, gene expression patterns, and differentiation. Using Strongy locentrotus purpuratus, the purple sea urchin, as their model system, Britten and Davidson explored how developmental processes are regulated by the differential activities of multiple sets of genes. In their exposition, they established a clear logical connection between regulatory changes in gene expression and its consequences on phenotypic variation, which redirected attention away from the consequences of individual mutations to the importance of changes in the patterns of gene network expression

The implications of this paradigm shift were immediately obvious to theorists—the genome became seen as an integrated regulatory system characterized by numerous possible interactions among modular components (now called gene regulatory networks , GRNs) affecting different aspects of differentiation and morphogenesis. An important implication of this paradigm was that GRNs were heritable units and that large-scale phenotypic changes could be the result of alterations in GRNs rather than the result of mutations affecting the code for structural proteins. In passing, it is worth noting that this perspective resonated with a much earlier and equally important conceptual shift, i.e., the transition from the Weltanschauung of Ernst Haeckel (1834–1919) to the world view of St. George Mivart (1827–1900). Haeckel’s Biogenic Law affirmed that “Phylogenesis is the mechanical cause of Ontogenesis” ( Haeckel, 1879 , p. 7; see Laubichler, 2010 ), whereas Mivart argued that changes in ontogeny are the central cause of evolutionary change ( Mivart, 1871 , pp. 233–234). Like Thomas Huxley, Mivart accepted evolution as a fact, but he rejected natural selection as the primary agency of evolution and speciation.

The homology–analogy paradox — It is certainly true that many of the architects of the modern synthesis recognized that the effects of genes are interactive and that continuously varying traits generally have a polygenic basis (e.g., Dobzhansky, 1970 ). However, the argument that modifications of developmental mechanisms are an important route to phenotypic novelty did not seriously inform the neo-Darwinian model in which gene mutation and natural selection sensu stricto continued to dominate thinking. Indeed, this argument even failed to convince no less an illustrious embryologist as Gavin R. de Beer (1899–1972) who wrote “It is now accepted that … mutations, and recombinations of genes … are responsible for the appearance of novelties in evolution” ( de Beer, 1958 , p. 22). In contrast, the rapid advances in molecular biological techniques following the Britten and Davidson 1969 paper had three longlasting effects: 

(1) they expanded the repertoire of organisms used to model the effects of developmental changes on evolution, 
(2) they allowed for increasingly broader comparative studies of GRNs, and 
(3) they permitted a refinement of earlier conceptualizations of the roles played by GRNs during the course of ancestor–descendant transformations. 

With continued advances, researchers began to see a pecking order in GRN importance in which some elements are highly conserved and thus shared across phyletically vastly different clades, whereas other elements performed multiple functions as “switches” or “input–output” circuits, and still others affected specific cell fates. In so doing, the privileged position of the gene was replaced by the privileged position of highly conserved GRN control elements called “generic toolkits”  and “kernels” .Perhaps the best known of these are the transcription factors that contain the more broadly distributed homeobox protein-binding DNA motif, which function in animal body axis patterning, and the MADS–box genes in fungi, plants, and animals, which have parallel functionalities. For example, the mouse and human Pax6 genes have extensive DNA sequence similarity  and function similarly upstream of the development of otherwise structurally very different kinds of eyes  including those of squids.

The discovery of extensive homologous molecular sequences participating in the development of structures that were classically considered to be analogous as opposed to homologous, as for example compound and camera eyes, was puzzling—so much so that it was referred to as the “molecular homology–analogy paradox” ( Wilkins, 2002 ; see also Newman, 2005 , 2006 ). As noted by Gehring (2002 , p. 69), “… there is no fundamental necessity to use a particular transcription factor for a particular function … since a transcription factor can regulate any gene”. This paradox was resolved by noting that molecular homology at the level of regulatory genes guarantees neither developmental nor phenotypic homology . Consider the ectopic expression of the normal form of ey in Drosophila and the normal Sey gene in mouse inserted into the fruit fly genome. Because ey and Sey retain their participatory function in the development of photoreceptors, the similarities of the observed phenotypes resulting from their expression indicates that these regulatory gene sequences have evolved little since the divergence of arthropods and chordates hundreds of millions of years ago. However, the gene networks targeted by ey and Sey have changed profoundly as have the morphological products resulting from their participation.
The evolution of transcription factors is further illustrated by the MADS box gene LEAFY ( LFY ), which is found in mosses, ferns, gymnosperms, and angiosperms. Among fl owering plants, the single LFY gene product binds to sequences in the enhancers of several homeotic fl oral genes (e.g., APETALA1 ). Among nonflowering plants, several LFY gene products control more general and numerous aspects of the life cycle. Thus, although the LFY DNA binding domain is strongly conserved across all plant taxa, the LFY protein as a whole has diverged in its functionality across taxa from mosses to angiosperms. This functional divergence is indicated by the ability of LFY cDNAs (isolated from mosses, ferns, and various gymnosperms linked to the Arabidopsis LFY promotor) to progressively recover the lfy mutant in Arabidopsis ( Maizel et al., 2005 ), i.e., the recovery pattern mirrors the phyletic distance of the LFY cDNA source from angiosperms. Two scenarios have been suggested to explain this phenomenology, both of which draw attention back to questions asked earlier in the introduction (i.e., is there a genomic toolkit or a set of “master genes” … and are they shared among all eukaryotic clades?). In the example given here, LFY either controls similar networks of genes that have coevolved with target genes that have themselves become modifi ed during plant diversifi cation, or the function of LFY in the different embryophyte lineages has changed completely as a result of the recruitment or intercalation of new target genes. In either case, the biology LFY illustrates that molecular homology neither guarantees nor intrinsically reveals morphological homology and that the meaning of phrases such as “shared toolkits” and “master genes” is ambiguous at best.


Modules — A question asked earlier was: Are the multiple origins of multicellularity truly independent given that all eukaryotes ultimately shared a last common ancestor? We can examine this question by noting that the molecular homology– analogy paradox is easily turned on its head. That is, the developmental mobilization of very dissimilar molecular systems or processes can produce much the same phenotypic effects. This dictum has been formalized by Newman and coworkers who proposed a framework for conceptualizing the development and evolution of multicellular animals based on dynamical patterning modules (DPMs), each of which involves one or more sets of shared gene networks, their products, and physical processes common to all living things  ;. Although the importance of some of these physical processes (e.g., cohesion, viscoelasticity, diffusion, and activator–inhibitor Turing dynamics) has been known for a long time, experimental work continues to show more elaborate phenomenologies such as how the mechanical environment experienced by the extracellular matrix can alter gene expression patterns and thus cell fate by changing the physical properties of the nuclear membrane. Within the DPM framework, physical generic processes operating in tandem with developmental modules can act in isolation or in combination to give rise to a “pattern language” for the formation of the basic body plans of multicellular animals. “Generic” in this context refers to a causal explanation predicated on mechanical forces due to the geometrical arrangements of mesoscale materials, abstract properties of network organization, symmetry breaking, or irreversibility. An explanation is generic because it can apply to living as well as nonliving phenomena. The generic nature of the physical processes associated with DPMs makes it theoretically possible for an assortment of stereotypical forms to emerge rapidly once multicellularity was achieved by metazoans, particularly since some DPMs can originate by the co-option of genes or gene regulatory networks present in unicellular or colonial organisms. For instance, neuropeptide and glycosphingolipid metabolism genes previously found only in metazoans are reported for the colonial choanoflagellate Salpingoeca rosetta, whereas the molecular components required for the polarization of cell layers with adherens junctions are reported for the demosponge Amphimedon queenslandica.  In theory, these DPMs or their analogues can operate in plants and fungi as well as animals because of fundamental similarities among all eukaryotic cells. Consider for example cell-to-cell adhesives. All eukaryotic cells have the capacity to secrete polysaccharides and structural glycoproteins that self-assemble to form extracellular matrices around animal and plant cells. Both types of matrices contain interpenetrating polymeric networks that employ hydroxyproline- rich glycoproteins (HRGPs) as major scaffolding components (collagen in animals and the HRGP extensin superfamily in various algae and in the embryophytes). These proteins generally form elongated, flexible, rod-like molecules with marked peptide periodicity (much like the modularity seen in mussel adhesives) with repeat motifs dominated by hydroxyproline in a polyproline II helical formation extensively modified by arabinosyl/galactosyl side chains. It is possible therefore that this “superfamily” of cell-to-cell adhesives evolved by the co-option of an ancestral gamete–gamete self-recognition or cell-adhesionto- substratum toolkit. Likewise, the evolutionary expansion of pre-existing gene families encoding regulatory proteins in combination with novel physical and regulatory interactions resulting from such expansions may also have played critical roles and may even have driven the evolution of multicellular complexity

The key issue here is, that these regulatory proteins had different regulation programming. The transition of regulation of one organism to another must be exact and fine-tuned. The question is how this could have happened by natural undirected means by evolution and natural selection.

as illustrated by the basic helix-loophelix (bHLH) protein family involved in diverse cellular developmental processes in plants and animals and a wide array of microtubule-associated proteins in algae, embryophytes, fungi, and metazoans. Nevertheless, the DPMs identified by Newman and coworkers cannot be applied directly to plant or fungal development because of substantive differences among these three major eukaryotic
clades . For example, during animal development, cells are typically free to migrate and slide past one another in ways that permit differential adhesion, cortical tension, and other processes that can facilitate the sorting
and assembly of some tissues, e.g., differences in CAM and P-adherin promote cell sorting during in vitro (but not in vivo) Xenopus gastrulation. In contrast, plant cells are characterized as having rigid cell walls that are typically firmly fixed to one another. Plant signaling molecules can also act intercellularly as well as intracellularly as transcriptional modulators and determinants of tissue as well as cell fate thereby blurring the functional separation of gene regulatory networks affecting multi- as opposed to single-cell differentiation. Although the intercellular transport of developmental transcription factors is not unknown in animal systems, it is very rar. Further, cell polarity in plants involves PIN and PAN1 proteins, whereas animal cell polarity involves integrin, cadherin, and PAR or CDC42 proteins  . Finally, cell division mechanics and the deposition of cell walls differ even among closely species in the same lineage, as for example in different desmids and in different filamentous ascomycetes . In light of these and other issues, Hernández-Hernández et al.
(2012) proposed a preliminary set of six DPMs associated particularly with critical embryophyte developmental processes:

(1) the formation and orientation of a future cell wall (FCW),
(2) the production of cell-to-cell adhesives (ADH),
(3) the formation of intercellular lines of communication and spatial-dependent patterns of differentiation (DIFF)
(4) the establishment of axial and lateral polarity (POL)
(5) the creation of lateral protrusions or buds (BUD), and
(6) the construction of appendicular leaflike structures (LLS).

For the purposes of this review, only the first four of these modules (i.e., FCW, ADH, DIFF, and POL) are relevant because cell-to-cell adhesion and intercellular communication are the condicio sine qua non of simple multicellularity across all eukaryotic clades and because these modules operate in a pairwise manner in many multicellular algae and fungi as well as in the land plants ( Fig. 3 ).

For example among embryophytes, the ADH and FCW modules operate in tandem because the presence of adhesive pectin polysaccharides in the middle lamella is associated with the deposition of the future primary cell walls of adjoining cells. The cell wall begins to be formed from cell plates during cytokinesis, such that cell adhesion is the default state    ( Fig. 4A, B ). Additionally, the proportion and chemical state (e.g., level of esterification) of each of the cell wall components is spatiotemporally regulated over the course of development, locally as well as globally, adjusting the mechanical properties of cells and tissues and contributing to the regulation of cell and organ growth in size, as well as to organogenesis. A somewhat analogous system operates during the extension of fungal hyphae ( Fig. 4C ; see section Cytokinesis and cell wall deposition ). The DIFF and POL modules are also functionally interconnected because both are required for cell-type specification and intercellular communication. For example, among embryophytes, DIFF and POL involve the transport of metabolites, transcription factors, and phytohormones through plasmodesmata. In some developmental systems, plasmodesmata also enable a type of generic physicochemical reaction–diffusion patterning mechanism that includes lateral inhibition mechanisms. Experimental evidence in A. thaliana and other model systems likewise shows that auxin flow and cell wall mechanical forces reciprocally interact during the emergence of polarity, whereas auxin promotes polar expansion by localized cell wall loosening, involving the acidifi cation of the apoplast and the concomitant disruption of noncovalent bonds among cell wall polysaccharides . The preferential localization of PINs (or their transporting vesicles) that determines auxin fluxes also targets loci for future cell wall loosening. Among animals, cell polarity has been extensively studied in the context of PAR proteins, the atypical protein kinase C (aPKC), and other proteins such as the small G protein Cdc42 as well as the roles played by the position and orientation of the mitotic spindle that in turn depend on heterotrimeric G protein signaling and the motor protein dynein. For example, ASIP/PAR-3, PAR-6, and aPKC form complexes that participate in the formation of the tight junctions in mammalian epithelial cells. These junctions establish the apical and baso-lateral domains of the epithelium that limit the movement of plasma membrane proteins. Each of the FCW, ADH, DIFF, and POL modules involves the participation of generic physical mechanisms such as mechanical forces. Consider for example how the FCW module operates in embryophytes in response to mechanical stresses. Centrifugation experiments of both haploid and diploid land plant cells show that the position of the interphase nucleus (which prefigures the preprophase band and the phragmoplast) establishes the location of the future division plane. On the basis of these and other observations, embryophyte cell division involves a microtubule (MT)- length-dependent force-sensing system that permits the cytoskeleton to position the nucleus (and thus the preprophase band) into a mechanically equilibrated location ( Fig. 5 ).

If the nucleus in interphase is positioned artificially off-center, the MTs radiating from it, outward to the cell cortex, will recenter the nucleus based on differences in the tensile forces generated among the MTs differing in length. Collectively shorter as opposed to longer MTs would be favored to achieve an equilibrium configuration that would axiomatically coincide with the minimal area plane. This model accords nicely with Hofmeister’s (1863)
and Errera’s (1888) rules, both of which identify the location and orientation of the new cell wall based on simple geometric rules. Cells that are too large would have MTs that would be unable to tether the nucleus to some cell wall facets; cells that are too small would have MTs experiencing compressive rather than tensile forces. Clearly, genomic components are required for the operation of the FCW module as revealed by the persistent participation of subfamily III leucine-rich repeat-receptor-like kinases in symmetric and asymmetric cell division. Thus, organisms may rely on physical forces to establish a simple default developmental condition, but they must modify their responses to these forces to achieve alternative developmental options. This is illustrated by how cell wall stresses induce the synthesis of different chitin synthase enzymes to rescue alternative septation and cytokinetic patterns in mutated yeast cells, or how the formation of the structures prefiguring the appearance of villi in the gut of the chick embryo relies on compressive mechanical forces generated by the differentiation of nearby smooth muscle tissue that cause the buckling of endoderm and mesenchyme

Mapping modules into morphospaces — The roles of the FCW, ADH, DIFF, and POL modules played during the evolution of multicellularity are shown when their functionalities are mapped onto a morphospace identifying the major plant body plans and when this map is informed with a series of morphological transformations predicted by a simple multilevel selection model for the evolutionary appearance of multicellularity. In general terms, a morphospace is a representation of all of the theoretically possible phenotypes within a specific group of organisms. Each axis defining the domains within a morphospace represents a developmental variable or process that describes or obtains a phenotypic character (with one or more character states). Each intersection of two or more axes identifies a hypothetical phenotype with the character states specifi ed by the variables or processes
stipulated by the participating axes. A morphospace for plant body plans was constructed previously using four developmental axes, each with two character states: 

(1) whether cytokinesis and karyokinesis are synchronous, 
(2) whether cells remain aggregated after they divide, 
(3) whether symplastic continuity or some other form of intercellular communication is maintained among neighboring cells, and 
(4) whether individual cells continue to grow indefi nitely in size ( Fig. 6 ). 

The intersections of these axes identify four major body plans, each of which can be theoretically either uninucleate or multinucleate: 

(1) the unicellular body plan, 
(2) the siphonous/coenocytic body plan, 
(3) the colonial body plan, and 
(4) the multicellular body plan. 

The addition of a fifth axis—the orientation(s) of cell division—distinguishes among the various tissue constructions of the multicellular plant body plan: 

(1) the unbranched filament, which results when cell division is confined to one plane of reference, 
(2) the branched filament (with or without a pseudoparenchymatous tissue construction), which requires two planes of cell division, and 
(3) the parenchymatous tissue construction, which requires three planes of cell division ( Fig. 7 ).

A review of the secondary and primary literature treating the algae  shows that all but two of the 14 theoretically possible phenotypes are represented by one or more species. It also reveals considerable homoplasy among various plant lineages. For example, the unicellular multinucleate variant with determinate growth is represented by the chlorophycean alga Bracteacoccus and the ulvophycean alga Chlorochytridium ; the colonial multinucleate body plan is represented by the chlorophycean algae Pediastrum and Hydrodictyon ; the siphonous body plan is represented by the ulvophycean alga Caulerpa and the xanthophycean alga Vaucheria ; and the multicellular multinucleate (siphonocladous) branched variant is represented by the rhodophycean alga Griffithsia and the ulvophycean alga Cladophora . Among the multinucleate multicellular (siphonocladous) variants differing in tissue construction, the unbranched and branched filamentous variants are represented by the ulvophycean algae Urospora and Acrosiphonia , respectively; the siphonocladous body plan with a pseudoparenchymatous tissue construction is represented by species within the ulvophycean genus Codium


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7 Origins of multicellularity on Sat Oct 03, 2015 9:21 am


Origins of multicellularity 1)

Interpreting truly ancient fossils is an especially tricky business. The conclusion that 2.1-billion-year-old structures from Gabon are the remains of large colonial organisms will get palaeobiologists talking.

It is a peculiar but widely held view that Charles Darwin used the palaeontological record as one of the principal lines of evidence for biological evolution. He did not. To modern eyes, On the Origin of Species presents a shocking account of the fossil record as an archive of evolutionary history. For instance, Darwin highlights the idea that the then earliest-known fossil-bearing rocks, from the Cambrian period, beginning about 542 million years ago, contain records of modern groups — implying an extensive prehistory teeming with life. One-and-a-half centuries of subsequent research have revealed a vast microscopic fossil record of unicellular protists and bacteria extending, some would argue, as far back as there are sedimentary rocks from which they could be recovered. But although fossils of millimetre- to metre-scale multicellular organisms characterize the 90 million years of the Ediacaran period that precedes the Cambrian, pre-Ediacaran macroscopic fossils are exceedingly rare. Hence the excitement that will surround the report on page 100 of this issue1, in which El Albani and colleagues describe macroscopic fossils from 2.1-billion-year-old rocks from southeastern Gabon. These centimetre-scale fossils, which the authors interpret as representatives of multicellular organisms, push the record of macroscopic life back more than 200 million years into the Palaeoproterozoic, an interval of Earth’s history so alien to us that we would not be able to breathe the air. Even though these fossils postdate the Great Oxidation Event — the notable rise in atmospheric oxygen 2.4 billion years ago — the atmosphere was still a toxic mix of greenhouse gases, with oxygen making up only a few per cent of modern levels. This bacterial world was undergoing the greatest episode of climate change in the history of the planet: pumping out oxygen, drawing down carbon dioxide, slowly transforming the Earth into the world we know. The fossils are not much to look at — yet, given their antiquity, the fact that they can be seen by the naked eye is astonishing. Out of their geological context, these structures are unremarkable and would probably have been ignored. But the geological context is as remarkable as are the potential evolutionary implications. El Albani and colleagues1 have, therefore, been painstaking in attempting to demonstrate the age and biological nature of the structures.

The rocks have been dated with great precision (to 2,100 ± 30 million years old), and the possibility that the structures are a younger mineral assemblage that grew within the rock has been excluded by sulphur-isotope analyses. These indicate that the fossil-replacing mineral pyrite (an iron sulphide) was precipitated by sulphate-reducing bacteria as the sediments were deposited. Further, contrasts between the carbon-isotope signature of the structures and their surrounding sediment indicate that the pyrite grew in an organic framework. However, it is the fossil morphology, revealed through X-ray microtomography, that provides the most compelling evidence of biogenicity. The fossils take the form of three-dimensional sheets with scalloped margins defined by radial slits and an internal radial fabric (as seen in Figure below).

The authors interpret this structure as evidence of coordinated growth. The relative complexity of the fossils, and their co-occurrence with soluble organic compounds containing sterane (derived from sterol precursors), lead El Albani and colleagues to conclude that they are unlik any living bacterium. They don’t rule out the possibility that these remains might even represent the earliest multicellular eukaryotes — that is, colonies of organisms with a membrane- bound nucleus that represent a distinct, more complex form of life from bacteria. The null hypothesis, however, has to be that these remains represent bacterial colonies. Future work must determine whether the sterane signature, a hallmark of eukaryotes, is derived from soluble organics generated within the sediments, or whether they migrated into these sediments from younger rock sequences. In the interim, however, is there anything in the geometry of these presumed multicellular sheets that sets them apart from bacterial colonies? Multicellularity represents one of the principal thresholds in evolutionary history 2. This threshold has been exceeded tens of times 3, perhaps because much of the requisite molecular machinery to facilitate cell–cell coordination is a shared primitive feature of living organisms 4, but also because some definitions of multicellularity encompass everything from simple bacterial colonies to badgers. Stricter definitions of multicellularity are met in far fewer instances. Although the fossils are macroscopic, they do not seem to represent anything other than the basic type of multicellularity, which occurs earlier in time in the form of stromatolites. Nevertheless, the size, form and thickness of these sheets may be significant. It has been argued that the paucity of ancient records of macroscopic multicellularity could reflect the physiological limitations enforced by atmospheric and oceanic chemistry during the first 2 billion years of Earth’s history5,6. The proximity in the age of these fossils to the timing of the Great Oxidation Event (Fig. below) fits elegantly with speculative hypotheses on the co-evolution of life and the chemistry of the oceans.

This latest discovery raises more questions than it answers. But within the confines of a very patchy global record of Proterozoic and Archaean rocks, which extend from about 3.8 billion years ago to the beginning of the Cambrian, these remains contribute to a fossil record that belies the dated caricature painted in the Origin. It was Darwin’s view that absence of organisms in these early intervals of Earth’s history would prove his theory of biological evolution wrong. The discovery and continuing elucidation of the Precambrian fossil record has met Darwin’s predictions on the extent and structure of evolutionary history.

1. El Albani, A. et al. Nature 466, 100–104 (2010).
2. Maynard Smith, J. & Szathmáry, E. The Major Transitions in
Evolution (Oxford Univ. Press, 1997).
3. Butterfield, N. J. Precambr. Res. 173, 201–211 (2009).
4. Shapiro, J. A. Annu. Rev. Microbiol. 52, 81–104 (1998).
5. Anbar, A. D. & Knoll, A. H. Science 297, 1137–1142 (2002).
6. Bengtson, S., Rasmussen, B. & Krapez, B. Paleobiology 33,
351–381 (2007).
7. Anbar, A. D. Science 322, 1481–1483 (2008).

Large colonial organisms with coordinated growth in oxygenated environments 2.1 Gyr ago 2)

The evidence for macroscopic life during the Palaeoproterozoic era (2.5–1.6 Gyr ago) is controversial 1–5. Except for the nearly 2-Gyr–old coil-shaped fossil Grypania spiralis 6,7, which may have been eukaryotic, evidence for morphological and taxonomic biodiversification of macroorganisms only occurs towards the beginning of the Mesoproterozoic era (1.6–1.0 Gyr) 8. Here we report the discovery of centimetre-sized structures from the 2.1-Gyr-old black shales of the Palaeoproterozoic Francevillian B Formation in Gabon, which we interpret as highly organized and spatially discrete populations of colonial organisms. The structures are up to 12 cm in size and have characteristic shapes, with a simple but distinct ground pattern of flexible sheets and, usually, a permeating radial fabric. Geochemical analyses suggest that the sediments were deposited under an oxygenated water column. Carbon and sulphur isotopic data indicate that the structures were distinct biogenic objects, fossilized by pyritization early in the formation of the rock. The growth patterns deduced from the fossil morphologies suggest that the organisms showed cell-to-cell signalling and coordinated responses, as is commonly associated with multicellular organization 9. The Gabon fossils, occurring after the 2.45–2.32-Gyr increase in atmospheric oxygen concentration 10, may be seen as ancient representatives of multicellular life, which expanded so rapidly 1.5 Gyr later, in the Cambrian explosion.

Our samples come from the Francevillian Group, which belongs to a well-recognized lithostratigraphic succession, outcropping across 35,000 km2 in southeastern Gabon11,12. This group is exposed in the intracratonic basins of Plateau des Abeilles, Lastoursville and Franceville , and reaches a maximum thickness of about 2,000 m.

Earliest multicellular life? 3) 

When people ordinarily think of multicellular organisms, they think of animals and plants (and fungi). Therefore, to hear that “multicellularity has evolved tens of times” gives the impression that it is a simple transition.

There is a fundamental difference between bacterial colonies, such as what the Gabon fossils most likely represent, and true multicellularity such as we find in animals, plants and fungi. Multicellularity as found in these latter organisms has four essential characteristics:14

-Genetic sameness throughout the cellular population to ensure every cell ‘plays by the same rules’.
-Physical cohesion between the cells such that separating some cells of from others causes severe injury or death to the organism.
-Intercellular coordination mediated through a cellular differentiation program for the development of the single cell zygote into a full-fledged multicellular individual.
-Repair and maintenance strategies, of which serial cell differentiation is the primary method, that work to maintain bodily integrity and control cellular selection  throughout the life of the organism.

Moreover, cells and organisms that don’t possess true multicellularity cannot decouple totipotency15 and immortality16 because they don’t already possess a full cellular differentiation program. And there is a fundamental conflict between cell-level and organism-level selection because competition for survival between individual cells is incompatible with the intercellular co-dependence of true multicellularity. All of these parameters and problems combined render the evolution of true multicellularity essentially impossible.17

Bacterial and unicellular eukaryotic colonies show widespread evidence of communication and coordination. However, like such colonies, there is no evidence of cell differentiation in the Gabon fossils, such as different tissue structures. Since cellular differentiation is the cornerstone of true multicellularity,18 the Gabon fossils remain mere colonial organisms and provide no evidence for the evolution of true multicellularity.

Problems with the timing of the fossils

In spite of all the confusion about “the evolution of multicellularity” regarding the Gabon fossils, Donoghue and Antcliffe claim:
“It was Darwin’s view that absence of organisms in these early intervals of Earth’s history would prove his theory of biological evolution wrong. The discovery and continuing elucidation of the Precambrian fossil record has met Darwin’s predictions on the extent and structure of evolutionary history.”
However, the researchers state that there is some superficial similarity to one dubious Ediacaran fossil. Nevertheless, this is as close as the researchers get to positing any concrete evolutionary links between the Gabon fossils and multicellular life. The obvious implication of thesuperficial similarity to a dubious Ediacaran fossil is that the researchers do not believe the Gabon fossils are ancestors of the Ediacaran biota. Therefore, we are still no closer to identifying the putative ancestors of the Ediacaran or Cambrian biota.

Moreover, these colonies are speculated to have gone extinct after the “Great Oxidation Event” (GOE) that supposedly occurred between 2.4 and 2.0 Ga ago.19 Despite the major problems with such a scenario,20,21 how does it provide anything new or exciting for evolutionary history? At best it’s a failed evolutionary experiment that wasn’t successfully replicated for another 1.5 Ga. At worst it’s another independent explosion of multicellular diversity with no antecedent evidence, just like the so-called Ediacaran and Cambrian ‘explosions’.22
Finally, colonial bacteria are a far cry from the intricate differentiation and body planning programs witnessed to in the Cambrian fossils. Therefore we are left with fossils with modern analogues (modern bacterial colonies) with no links to anything more advanced. Once again, the fossils appear fully formed, with no evidence of gradual transition in the rocks. This is a far cry from substantiating Darwin’s claims about the fossil record—rather, they falsify them.23

1) and 2) Nature Vol 466 | Issue no. 7302 | 1 July 2010

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Eukaryotes and the First Multicellular Life Forms 1

An important evolutionary innovation was multicellularity. The oldest known possible multicellular eukaryote is Grypania spiralis, a coiled, ribbon-like fossil two millimeters wide and over ten centimeters long.

Grypania spiralis was a coiled, spaghetti-like organism up to half a metre in length found in ~1300 Ma shales and slates from Montana, China and India.3

It is not known for certain what kind of organism this fossil represents, to which (if any) of the moden kingdoms it is most closely related, nor even if it was a large unicell – perhaps with many nuclei – or multicellular.

This is a specimen of 2.2 billion-year-old Grypania spiralis – the oldest known eukaryotic (multicellular) organism and one of the rarest fossils on Earth.  It is described as filaments of red algae from the middle Precambrian iron formations in upper Michigan (see Science, July 10, 1992, pp 232-235).  4

Grypania spiralis is by far the oldest known multicellular organism. All other Precambrian specimens of this age are prokaryotes (simple, single-celled organisms that lack a cellular nucleus) – such as stromatolites.   The discovery of Grypania in the 1980’s caused great excitement in the world of paleontology because these organisms are over 1 billion years older than the next-closest-aged eukaryote. This singularly unique anomalous occurrence of early eukaryotes continues to confound paleontologists today.

The development of eukaryotes (that is, cells which contain a nucleus) is one of the fundamental ‘great leaps forward’ in the evolution of life.  From this template all other complex life became possible. Grypania is a cornerstone in this field of research.

 It looks very much like a coiled multicellular alga and has been described from banded iron formations in Michigan 2.1 billion years old. Grypania may not be a eukaryote, but another, unrelated colonial eukaryote, Horodyskia, is known from sedimentary rocks dated at 1.5 billion years in western North America and from rocks more than 1 billion years old in Western Australia.

Multicellular fossils from 600 mya? 5

In an effort to determine how, why, and when multicellularity arose from single-celled ancestors, Xiao and his collaborators looked at phosphorite rocks from the Doushantuo Formation in central Guizhou Province of South China, recovering three-dimensionally preserved multicellular fossils that showed signs of cell-to-cell adhesion, differentiation, and programmed cell death — qualities of complex multicellular eukaryotes such as animals and plants.

Fossil of ancient multicellular life sets evolutionary timeline back 60 million years 2

A Virginia Tech geobiologist with collaborators from the Chinese Academy of Sciences have found evidence in the fossil record that complex multicellularity appeared in living things about 600 million years ago -- nearly 60 million years before skeletal animals appeared during a huge growth spurt of new life on Earth known as the Cambrian Explosion.

The discovery published online Wednesday in the journal Nature contradicts several longstanding interpretations of multicellular fossils from at least 600 million years ago.

"This opens up a new door for us to shine some light on the timing and evolutionary steps that were taken by multicellular organisms that would eventually go on to dominate the Earth in a very visible way," said Shuhai Xiao, a professor of geobiology in the Virginia Tech College of Science. "Fossils similar to these have been interpreted as bacteria, single-cell eukaryotes, algae, and transitional forms related to modern animals such as sponges, sea anemones, or bilaterally symmetrical animals. This paper lets us put aside some of those interpretations."

In an effort to determine how, why, and when multicellularity arose from single-celled ancestors, Xiao and his collaborators looked at phosphorite rocks from the Doushantuo Formation in central Guizhou Province of South China, recovering three-dimensionally preserved multicellular fossils that showed signs of cell-to-cell adhesion, differentiation, and programmed cell death -- qualities of complex multicellular eukaryotes such as animals and plants.

The discovery sheds light on how and when solo cells began to cooperate with other cells to make a single, cohesive life form.
The complex multicellularity evident in the fossils is inconsistent with the simpler forms such as bacteria and single-celled life typically expected 600 million years ago.
While some hypotheses can now be discarded, several interpretations may still exist, including the multicellular fossils being transitional forms related to animals or multicellular algae.

A fossil of a 600 million-year-old multicellular organism displays unexpected evidence of complexity.

Three-dimensional preservation of cellular and subcellular structures suggests 1.6 billion-year-old crown-group red algae 6
The ~1.6 Ga Tirohan Dolomite of the Lower Vindhyan in central India contains phosphatized stromatolitic microbialites. We report from there uniquely well-preserved fossils interpreted as probable crown-group rhodophytes (red algae). The filamentous form Rafatazmia chitrakootensis n. gen, n. sp. has uniserial rows of large cells and grows through diffusely distributed septation. Each cell has a centrally suspended, conspicuous rhomboidal disk interpreted as a pyrenoid. The septa between the cells have central structures that may represent pit connections and pit plugs. Another filamentous form, Denaricion mendax n. gen., n. sp., has coin-like cells reminiscent of those in large sulfur-oxidizing bacteria but much more recalcitrant than the liquid-vacuole-filled cells of the latter. There are also resemblances with oscillatoriacean cyanobacteria, although cell volumes in the latter are much smaller. The wider affinities of Denaricion are uncertain. Ramathallus lobatus n. gen., n. sp. is a lobate sessile alga with pseudoparenchymatous thallus, “cell fountains,” and apical growth, suggesting florideophycean affinity. If these inferences are correct, Rafatazmia and Ramathallus represent crown-group multicellular rhodophytes, antedating the oldest previously accepted red alga in the fossil record by about 400 million years.


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It all starts with multicellularity: 1 An article in PhysOrg based on work at the Salk Institute and the Joint Genome Institute makes multicellularity a cinch: it’s “all in the family.”  Work on Volvox led them to say, “One of the most pivotal steps in evolution—the transition from unicellular to multicellular organisms—may not have required as much retooling as commonly believed.”  They explained, “multicellular organisms may have been able to build their more complex molecular machinery largely from the same list of parts that was already available to their unicellular ancestors.”  That begs the question of where the unicellular ancestors got their complex molecular machinery, but hey: it’s just a matter of reorganizing the same Lego blocks, they said.  But if “Volvox, the most sophisticated member of the lineage, is believed to have evolved from a Chlamydomonas-like ancestor within the last 200 million years,” and if “In most cases the switch from a solitary existence to a communal one happened so long ago—over 500 million years—that the genetic changes enabling it are very difficult to trace,” how can they claim that with some green algae, “the transition to multicellularity happened in a series of small, potentially adaptive changes, and the progressive increase in morphological and developmental complexity can still be seen in contemporary members of the group”?  If most cases were long ago, why are there any today?  And if so little retooling is required, why is there not more multicellularity evolving right before their eyes?  They didn’t elaborate, but treated the origin of multicellularity as a stepping-stone to sex: “some subtypes evolved into a diffusible hormonal trigger for sexual differentiation,” the article ended, without explaining where the hormones came from.
    Elisabeth Pennisi’s coverage of this story in Science1 produced another conundrum.  She began by saying, “How a single cell made the leap to a complex organism is one of life’s great mysteries.”  Then she quoted David Kirk of Washington University at St. Louis saying, “Even major evolutionary transitions can be accomplished via relatively subtle genetic changes.”  But the very next sentence said, “As a result, solving this mystery ‘is going to take a lot more work.’”  How can it be a lot of work to study a simple, albeit subtle, genetic change?  She said they found “surprisingly few differences” between Volvox, a colonial organism, and Chlamydomonas, a unicellular species.  Although her article did not discuss the origin of sex, the theme was that major changes can accompany simple rearrangements.  Quoting Nicole King of UC Berkeley, “The key transition is not inventing a whole bunch of genes and proteins; you just have to change the way you use what you have.

Origins of multicellularity: All in the family 2

Volvox, the most sophisticated member of the lineage, is believed to have evolved from a Chlamydomonas-like ancestor within the last 200 million years, making the two living organisms an appealing model to study the evolutionary changes that brought about multicellularity and cellular differentiation. To gather data for the comparative genomic analysis, the researchers sequenced the 138 million base pair Volvox genome using a whole genome shotgun strategy. The genome itself is 17% larger than the previously sequenced genome of Chlamydomonas and the sequence divergence between the two is comparable to that between human and chicken. Volvox, the most sophisticated member of the lineage, is believed to have evolved from a Chlamydomonas-like ancestor within the last 200 million years, making the two living organisms an appealing model to study the evolutionary changes that brought about multicellularity and cellular differentiation. To gather data for the comparative genomic analysis, the researchers sequenced the 138 million base pair Volvox genome using a whole genome shotgun strategy. The genome itself is 17% larger than the previously sequenced genome of Chlamydomonas and the sequence divergence between the two is comparable to that between human and chicken. Despite the modest increase in genome size, the number of predicted proteins turned out to be very similar for the two organisms (14,566 in Volvox vs. 14,516 in Chlamydomonas) and no significant differences could be identified in the repertoires of protein domains or domain combinations. Protein domains are parts of proteins that can evolve, function, and exist independently of the rest of the protein chain. "This was somewhat unexpected," explains Umen, "since innovation at the domain level was previously thought to play a role in the evolution of multicellularity in the plant and animal lineages." In contrast to the overall lack of innovation, protein families specific to volvocine algae, such as extracellular matrix proteins, were enriched in Volvox compared to Chlamydomonas. Each mature Volvox colony is composed of numerous flagellated cells similar to Chlamydomonas, which are embedded in the surface of a spheroid of elaborately patterned extracellular matrix (ECM) that is clearly related to the Chlamydomonas cell wall. Maybe not surprisingly, the difference in size and complexity between the Volvox extracellular matrix and Chlamydomonas cell wall is mirrored by a dramatic increase in the number and variety of Volvox genes for two major ECM protein families, pherophorins and VMPs.
Additionally, Umen and his collaborators identified an increase in the number of cyclin D proteins in Volvox, which govern cell division and may be necessary to ensure the complex regulation of cell division during Volvox development. Last but not least, Volvox adapted a few of its existing genes to acquire novel functions. Members of the pherophorin family, for one, not only help build the extracellular matrix; some subtypes evolved into a diffusible hormonal trigger for sexual differentiation.


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10 Volvox on Sun Oct 04, 2015 5:09 pm


Genomic Analysis of Organismal Complexity in the Multicellular Green Alga Volvox carteri

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The Evolution of Early Animal Complexity 1

Differentiation is a key feature of multicellular life:

Emergence of a New Field: Evolution and Development (Evo/Devo) - new insights into the origin and evolution of multicellular organisms.

One of the main differences between unicellular and multicellular organisms is cell differentiation. That is, cells become specialized for a specific function and, usually, take on a characteristic morphology. For example, your body has epithelial cells lining most of its surfaces. If you take an epithelial cell and grow them in tissue culture they will multiply but they will remain epithelial cells.
How do cells get locked into one type? In the early 1900's, scientists suggested that the genes that control a particular kind of cell (such as an epithelial cell, for example) are passed on to those cells during development and all other genes (such as those that control muscle cells) are filtered out. As you well know, that isn't the case - each of your cells has all the genes needed to make an exact copy of you. This means that some genes are not used in some cells -- for example, muscle cell genes are not used in epithelial cells.
Cell differentiation then depends on different genes being active in different cells. This occurs through a process called gene regulation. In gene regulation, one gene (called a regulator gene) acts a a switch that turns other genes on or off. A basic version of this process occurs in bacteria and protists as well as multicellular organisms.
For example, use of the milk sugar lactose by E. coli in your digestive tract. E coli has three genes that produce enzymes to break down lactose and release ATP. These genes are preceeded on the DNA strand by a promoter (a base sequence that signals the start of a gene) and an operator (an intervening sequence with an active binding site):

Lactose isn't always present, so the bacterium does not need to make the enzymes necessary to break it down. The regulatory gene makes a repressor protein that binds with the operator and stops the production of the enzyme:

When lactose is present, it binds with the repressor protein so that the receptor site in the operator is empty, and the gene is transcribed:

You could also have an activator protein being made that turns an operator on rather than off.
Locking a cell into one type
In some protists (ciliates have been particularly well studied), some genes get turned off and stay off even after mitosis. The whole genome doesn't get reactivated until the protist goes through meiosis. This occurs when either a protein or a methyl group is added to the DNA blocking transcription of the gene at that site. When the DNA is replicated in mitosis, an enzyme copies the methyl group onto the new piece of DNA. When the cell goes through meiosis, however, the methyl groups are removed and the entire DNA is reactivated.

Master Control Genes of Differentiation

In the first steps of development in multicellular organisms, cells divide and spread but there is no differentiation. Embryos at this stage do, however, have an anterior to posterior gradient that appears to be inherited from the egg's cytoplasm. This gives the embryo an anterior "head" end and a posterior "tail" end. 
Cell differentiation is under the control of a set of master genes known as the Hox genes. The Hox genes are a family of genes arranged in a sequence on a chromosome. The anterior-most gene controls the head end of the body by regulating which genes in the anterior cells are activated and which are methelyated (and so turned off). Developmental biologists have investigated the role of these genes in embryos of fruit flies by turning hox genes on and off - for example, by turning off the first gene and turning on the second gene in the anterior end of the animal they can cause legs instead of antenae to grow out of the head.
All animals have Hox genes, but animals that evolve later have more genes and more complex, segmented bodies. Also the genes that are controlled change over time - it may be that the origin of new phyla occurs because of these switches.

B. Constraints

1. Size - 
As a body increases in size, the ratio of surface area to volume increases.

Volume increases by body length 3
Surface area increases by body length2

In small animals the surface area is great enough in proportion to the volume to exchange gases and waste by diffusion as well as move nutrients around the body by diffusion.

Larger animals must have organ systems to pump gases and wastes in and out (e.g., such as a circulatory system).

2. Habitat - animals that live in marine water are isotonic with it; animals that live in freshwater must have a system of eliminating the water that leaks into their body by osmosis (they have an internal concentration of salt higher than the surounding environment); terrestrial animals must cope with drying conditions.

Body weight in and out of water

Protect gametes in and out of water

wastes in and out of water

3. Speed of locomotion

Sessile (not moving) or slow moving animals must be aware of potential predators or prey moving in on any side, so they are often radial or bi-radial in symmetry

Rapidly moving animals must be more concerned about the environment that they are moving into, so they often have bilateral symmetry with cephalization (a "head end").

This, in turn will affect how an animal feeds: a motile animal can move towards food; a sessile animal has to bring the fodd to itself (by setting up a water current, for example).
But organisms also carry "phylogenetic baggage" - for example a sessile vertebrate will tend to have more radial symmetry, but it will still have bones!

A twelve-step program for evolving multicellularity and a division of labor 1


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Evolution of multicellularity: what is required? 1

All evolution assumes either the augmentation of some prior system to fit a new need, or lateral gene transfer adding information for the same end. Even systems that seem to require completely new structures (feathers for example) are assumed to be modified from pre-existing structures. However, there are two significant events in evolutionary history where far more would have been required—the origin of life, and the origin of co-ordinated multicellularity.

Requirements for multicellular evolution Genetic sameness

The first requirement for multicellularity to emerge is that all the cells must contain the same genetic information. Wolpert and Szathmáry provide a good overview of why genetic sameness is required for a multicellular organism to be viable as an individual:

‘The first step in the development of a complex organism is the establishment of a pattern of cells with different states that can differentiate along different pathways. … [P]atterning processes require signalling between and within cells, leading ultimately to gene activation or inactivation. Such a process can lead to reliable patterns of cell activities only if all the cells have the same set of genes and obey the same rules [emphasis added].’1

Without the same genetic blueprint to work from, there is no guarantee that cells will be able to communicate properly so as to co-ordinate their actions.

A new level of biological organisation

Evolution requires more than a mere augmentation of an existing system for co-ordinated multicellularity to evolve; it requires the ex nihilo creation of an entirely new system of organisation to co-ordinate cells appropriately to form a multicellular individual. Nedelcu and Michod concur:

‘The current hierarchical organization of life reflects a series of transitions in the units of evolution, such as from genes to chromosomes, from prokaryotic to eukaryotic cells, from unicellular to multicellular individuals, and from multicellular organisms to societies. During these evolutionary transitions, new levels of biological organization are created [emphasis added]’.2

Williams talks of the irreducible structure of the cell, and finds a universal example in autopoiesis (self-making).3 He describes five levels of organisation in all living things that are needed for autopoiesis to occur:

-Perfectly-pure, single-molecule-specific biochemistry. 
-Molecules with highly specific structures. 
-Highly structured molecules that are functionally integrated
-Comprehensively regulated information-driven metabolic processes
-Inversely-causal meta-informational (information about information) strategies for individual and species survival.
-Moreover, each level is greater than the sum of the levels that make it up such that the only way these levels can be explained is by information.

‘Each level is built upon, but cannot be explained in terms of, the level below it. And between the base level (perfectly pure composition) and the natural environment, there is an unbridgeable abyss.’4

To Williams’ autopoietic hierarchy, I wish to add another level of structure found only in multicellular organisms: intercellular co-ordination. The organism has strategies for arranging and differentiating its cells for survival and reproduction. With this comes a communication network between the cells that regulates the positioning and abundance of each cell type for the benefit of the whole organism. A fundamental part of this organisation is cellular differentiation, which is ubiquitous in multicellular organisms. This level cannot be explained by the sum of the parts, cells, and requires co-ordination from an organisational level above what exists in individual cells.
Biologist Eric Davidson5 identifies a 4-level hierarchy of control in multicellular organisms that constitutes a gene regulatory network. This gene regulatory network is essential for the development of the single cell zygote into a full-fledged multicellular individual. To put it in an approximate Linnaean framework, the hierarchy consists of 

-kernels6 that roughly determine phylum body plan, 
-plug-ins7 and input/output linkages8 that approximately determine class, 
-order and family body structure, and
-differentiation gene batteries9 that carry out the terminal stages of development and contribute to variation at the genus and species level.

Repair and maintenance strategies

Repair and maintenance strategies are integral for the survival of the adult multicellular individual because cellular selection operates with cell populations, including multicellular organisms, to select for the most reproductively aggressive cells. This needs to be controlled at the organismal level to maintain bodily integrity. To do this, most systems in multicellular animals undergo a process of serial differentiation.10In this system, multipotent11 stem cells are essential, though maintained at low population levels.

Cellular selection vs organismal integrity 12

Evolution faces a tough dichotomy to get around if multicellularity is to evolve: cellular selection vs organismal integrity. At the single cell level, selection will favour cells that reproduce better. But if those cells are allowed to reproduce uncontrollably in a multicellular organism, they will inexorably destroy organismal integrity, and harm or kill the organism, also causing the ‘fitter’ cells to die.13
At the organismal level, selection will favour traits that preserve organismal integrity, which tries to control reproduction of cells beyond what is needed. Pepper et al. agree:

‘Multicellular organisms could not emerge as functional entities before organism-level selection had led to the evolution of mechanisms to suppress cell-level selection.’14

However, this leads to a mystery for the evolutionist: how do multicellular organisms evolve from single celled creatures when cellular selection and organism-level selection are totally contradictory to each other? The multicellular organism seeks to control the reproduction to what is needed at a higher level of organisation; a single cell seeks to reproduce more than its competitors.
It appears that mechanisms for apoptosis (programmed cell death) are necessary for multicellularity, whereby certain cells are triggered to die during development or because they have gone haywire. Such mechanisms are incredibly complex and arguably irreducibly complex.15Explaining the existence of such a mechanism without intelligent design seems to be a futile exercise.16

Co-operation and colony: halfway there?

Co-operative and colonial organisms are proposed to be the route through which multicellularity evolved. Cooperative behaviour occurs in unicellular organisms. For example, Salmonella typhimurium can arrange themselves in two ranks for invasion—the first rank launches a suicide attack and the second rank slips through the confusion in the defence caused by the first wave.17 Therefore, some communication between unicellular organisms occurs to allow for co-operation.
Many organisms form colonies. However, single cells in most of these colonies retain the ability to ‘break off’ from the colony when circumstances are favourable to doing so. Colonial systems have co-operation, but no regulatory system to force the cells together as a unit of selection in its own right. Moreover, a colonial organism can be pulled apart without significantly damaging it, unlike a multicellular organism, which will be severely injured or die if pulled apart. Michod et al. concur:

‘Such associations and groups may persist and reform with varying likelihood depending on properties of the group and the component individuals. Initially, group fitness is the average of the lower-level individual fitnesses, but as the evolutionary transition proceeds, group fitness becomes decoupled from the fitness of its lower-level components. Indeed, the essence of an evolutionary transition in individuality is that the lower-level individuals must “relinquish” their “claim” to fitness, that is to flourish and multiply, in favor of the new higher-level unit.’18

‘The un-coupling of immortality and totipotency proved not possible in V. carteri: these traits are express either together and fully (i.e. in the gonidia) or not at all (i.e. in the somatic cells). Immortality and totipotency are thus still tightly linked inV. carteri, as they are in their unicellular ancestors. In support of this view is the fact that “cancer-like” mutant somatic cells, in which immortality but not totipotency is re-gained, are missing in V. carteri. There are, however mutant forms of V. carteri … in which somatic cells re-gain both immortality and totipotency, but in neither of these mutants are the two traits expressed partially or differentially (e.g. limited mitotic capacity or multipotency).’21Some colonial organisms, however, do appear to be obligate and show some specialisation, such as some members of the Volvolaceae family, like Volvox carteri. The point at which colonial organisms fail as true multicellular organisms is their lack of division of totipotency19 and ‘immortality’:20
This means that differentiation in the colony could only extend to two different types of cells and no further. Because they are unable to split totipotency and immortality, volvocine algae cannot create new somatic cells, and are as a result unable to survive for very long as an organism. In other words, there are no maintenance or repair strategies in volvocine life forms, so they lack one of the essential features of true multicellularity.

Opportunities for further research

I’ve here tried to present some basic requirements that must be met for the evolution of true multicellularity. For true multicellularity there has to be genetic sameness among all participating cells. Intercellular co-ordination serves as another level of organisation in life that can’t be reduced to the sum of its parts. There is a 4-level hierarchy in the regulatory architecture that must all be there for a viable developmental plan to proceed. Repair and maintenance requires one or more pools of undifferentiated, generally multipotent, stem cells. Cellular selection and organismal integrity remain diametrically opposed, and provide a very tough problem for evolution to overcome. Colonial unicellular organisms don’t fit the bill as multicellular creatures because of the difference between of their lack of this 4-level hierarchy, and the lack of maintenance and repair mechanisms for the organism. This is a neglected area of creationist research, where there are a number of opportunities for further investigation

Serial cell differentiation: intricate system of design 2

Single celled organisms replicate as fully functional cells, and they maintain cellular integrity through a system of direct epigenetic inheritance,1 or ‘cell memory’. Some tissues in multicellular organisms proliferate in the same way. However, the majority of tissues in adult multicellular organisms don’t.

Figure 1. The process of hematopoiesis (the generation of blood cells) is an example of the serial cell differentiation process.

Most tissues in mature multicellular organisms replicate via a method called serial differentiation.Cells go through a series of differentiation stages as they duplicate, ending in a fully differentiated cell, which eventually dies and passes out of the system, or is recycled by apoptosis (programmed cell death). There are three different types of cells in this system: 

- stem cells, a class called 
-‘transient amplifying cells’ (TACs) and 
- fully differentiated cells.

Serial differentiation

Stem cells

The undifferentiated cells are the only ones in this differentiation process that are self-renewing, i.e. they produce daughter cells that are exactly like the mother cell. These cells have the capacity to divide and change into many different types of cells. They are also very important during embryonic development, where new cell types are constantly needed.3 These stem cells are kept relatively few in number, and the cell lines proliferate through the differentiation process.

Transient amplifying cells

The daughters of stem cells do more than just self-renew; they differentiate into different kinds of cells. However, they don’t change into fully differentiated cells immediately; they change into a class called ‘transient amplifying cells’ (TACs). While TACs divide; unlike stem cells, TACs do not self-renew. Rather, the daughter cells of TACs are one stage further along the differentiation process than the ‘mother’ cell. These cells amplify the number of cells that will eventually become fully differentiated from the original stem cell that they started from.

Fully differentiated cells

A particular stem cell goes through a number of cell division events and the differentiation process of the TAC stage to produce fully differentiated cells. These are the mature cells that carry out the different jobs of the tissues, such as blood cells (figure 1), reproductive cells and epithelial cells. These cells no longer divide or differentiate, and once they have served their purpose, they are ‘deleted’ from the system and their components are recycled.4

Designed for maintenance

As Pepper et al. point out, the aim of this process is to separate the self-renewing and active proliferating properties of cells into different groups.2 This severely limits the number of duplications that any one cell line will undergo, which limits the possibility of mutational damage taking hold in a particular tissue.This is a rather elaborate system to conjure up if you just want to maintain tissues! It is also metabolically expensive because not only do the mature cells require nutrients, but so do the stem cells and TACs. Therefore, you’re feeding cells that don’t actually do anything in the body except replicate. So why bother using so much energy?
This system actively works against natural selection of individual cells in favour of tissue integrity to suppress somatic evolution, which is the change that the body is subjected to due to mutation and selection within the body’s cell population. Pepper et al. comment:

“We hypothesize that this is achieved in animals by compartmentalizing self-renewing tissues such that one cell population (stem cells) undergoes self-renewal, while another (TACs) undergoes active proliferation. If no cell population combines both these necessary elements of somatic evolution, somatic evolution is thereby suppressed.”

The stem cells are maintained as a small and quiescent population through slow self-renewal. The maintenance of the self-renewing population at low levels militates against selection of highly proliferative strains of stem cells.
The later stages of the differentiation process are focussed on proliferation, but they don’t self-renew. Each duplication event moves the daughter cells along the next stage of differentiation, until the cells are shed after they have become fully differentiated.
While it would cost less energy to just have self-renewing mature cells, it would result in the quick death of the organism if something went wrong in comparison to serial differentiation.
Less energy would be used up because the body would not have to support stem cells and TACs, but only fully differentiated cells. However, there is a much higher chance a mutation that increases the reproductive success of a particular cell would gain a hold in such a setup when compared to serial differentiation. Therefore, the benefit of longevity far outweighs the energy cost incurred for maintaining the system.

Evolution of multicellularity and serial differentiation

Pepper et al. also comment on the prospects of serial cellular differentiation aiding the transition from unicellular to multicellular life:

“It is believed that multicellular organisms could not have arisen or been evolutionarily stable without possessing mechanisms to suppress somatic selection among cells within organisms, which would otherwise disrupt organismal integrity. Here, we propose that one such mechanism is a specific pattern of ongoing cell differentiation commonly found in metazoans with cell turnover, which we call ‘serial differentiation’.”5

They believe that this transition from unicellularity to multicellularity is controlled by epigenetic alterations:

“Thus, our results support the suggestion…that epigenetic inheritance played a central role in the transition from unicellular to multicellular life by helping to control selection among the cells of the newly emergent multicellular individual.”5

However, both serial differentiation and the multicellular organism have to be assumed for this to work. At best it suggests how multicellularity persisted, but it does not suggest its origin. There is a fundamental evolutionary conflict in a multicellular organism: cellular selection vs bodily integrity. Generally, natural selection at the cellular level will favour those cells that are better at reproductive competition and survival. However, if those cells are allowed to proliferate in an uncontrolled manner in a multicellular organism, it will inevitably disrupt the organism’s bodily integrity, and harm or kill the organism.6 This inevitably kills these ‘fitter’ cells too because they cause the host to die. Cancer is a prime example. A cancer is essentially a mess of excessively proliferating cells within a multicellular organism. In an environment with limited resources (the organism), such cells will naturally out-compete normal cells because normal cells generally don’t proliferate indefinitely. The cancer cells outstrip the normal cells for resources and take over the system. However, this leads to malfunction in the organism, and if left untreated, will inevitably kill the organism. At the organismal level, selection will favour those traits that preserve bodily integrity, which seeks to control proliferation of cells beyond what is necessary. Pepper et al. confer:

“Multicellular organisms could not emerge as functional entities before organism-level selection had led to the evolution of mechanisms to suppress cell-level selection.”7

“Even today, apoptosis serves an essential role in terms of ‘cellular altruism’. It helps to ensure that an organism’s genetic integrity is not compromised, by removing some somatic cells that have sustained irreparable, genetic mutations. Crucially, apoptosis also helps to maintain a species’ genetic integrity, by eliminating aberrant germ cells that would otherwise carry intact but faulty genes into the next generation.”8However, this leads to a conundrum for the evolutionist: how do multicellular creatures evolve from single celled organisms when cellular selection is diametrically opposed to organism-level selection? A single cell seeks to proliferate more than its competitors; the multicellular organism seeks to control such proliferation to what is needed at a higher level of organisation. This can be seen in the process of apoptosis as well: The system of serial differentiation is designed to enhance bodily integrity, not reduce it. The system has to be in place before it can be selected for, yet organism-level selection cannot take over without measures such as serial differentiation in place. The very existence of this system argues against the evolution of multicellularity.


Serial differentiation is an essential system for the maintenance of mature multicelled organisms. It serves to separate the self-renewal and proliferative stages of cell division, which limits the effect mutations have on tissues. Evolution cannot explain the origin of the system, and neither can it explain the origin of multicellularity. These features of life clearly speak of purposeful, intelligent creation consistent with the Bible’s account of creation.

Does biological advantage imply biological origin ?3

The origins of sexual dimorphism and multicellularity are two of the greatest mysteries to evolution. For either of them to evolve requires massive restructuring of the biological system from the molecular to the organismal levels. Moreover, there are massive selection and energetic barriers that must be crossed to get from unicellular to multicellular life and to evolve sexual dimorphism. Two recent news articles have claimed that certain biological advantages in sexual dimorphism1 and multicellularity2 provide a reason why they evolved in the first place.

Intra-cell communication and sexual dimorphism

The first study discusses the question: why are there two sexes?3 In terms of evolution, it’s not the best number of mating types because it only allows us to mate with half of the population. However, researchers have proposed that inheriting mitochondrial DNA (mtDNA) from just one parent instead of both may serve to offset this disadvantage. Most sexually reproducing creatures only receive nuclear DNA from their father but get the other half of their nuclear DNA plus their entire cellular structure, including mtDNA, from their mother. The researchers proposed that because this setup only passed one set of mtDNA to offspring, it allowed for more efficient ‘synchronization’ between the nucleus and mitochondria, and between mitochondria, than would be possible if mitochondria were inherited from both parents. According to their modelling, they were correct—uniparental inheritance of mitochondria (UIM) produced fitter offspring than biparental inheritance of mitochondria (BIM) under most realistic selection constraints.
Evolution is taken as so incontrovertible that questions of how (the succession of evolutionary events) are deemed superfluous, and all that matters is why.
But the researchers also explore this question: “Could uniparental inheritance of mitochondria have arisen to facilitate better co-adaptation of mitochondrial and nuclear genes, and so explain the evolution of two sexes?”,3 to which they ultimately give a positive answer. However, this misplaces the important question for the evolution of any new trait—how it arose in the first place. Essentially, they perform a cost-benefit analysis between UIM and BIM, determine that UIM is the better system, and then conclude that UIM must have evolved from BIM. But this skips over the succession of events that supposedly led to the evolution of UIM from BIM because the researchers assume that since UIM and sexual dimorphism exist, they must have evolved. This is clearly begging the question of evolution, but it’s worse. Evolution is taken as so incontrovertible that questions of how (the succession of evolutionary events) are deemed superfluous, and all that matters is why UIM evolved. However, all they have established is that UIM provides the functional grounds for sexual dimorphism in eukaryotes, and the origin of that function is the very question which the fact of its functionality does not directly address.

Kinship and the evolution of multicellularity

Another recent study showed how high-relatedness between cells is a necessary prerequisite for multicellularity.4The researchers ran two experiments on the amoeba Dictyostelium discoideum, one where they tested the effects of low-relatedness on Dictyostelium’s ability to form multicellular fruiting bodies, and the other tested the effects of mutation accumulation in a single clonal line. The researchers found that when different lines were mixed, it didn’t take long for ‘cheater’ mutants to take advantage of the fruiting bodies and propagate ahead of the non-cheaters, to the point where there were so many ‘cheaters’ that many lines were unable to form fruiting bodies at all by the end of the experiment. In contrast, fruiting ability was never lost in the mutation accumulation experiment where high-relatedness was maintained, as per conditions in the wild. As a result, the researchers concluded that high-relatedness was necessary and sufficient to maintain the viability of the multicellular stage inDictyostelium’s life cycle. The researchers then applied their findings to multicellular life in general:

“Thus, we conclude that the single-cell bottleneck is a powerful stabilizer of cellular cooperation in multicellular organisms.”5

This is a fair application of their research. It highlights a necessary prerequisite for functional multicellularity, and it doesn’t extend all the conclusions about high-relatedness in Dictyostelium to all multicellular life. But compare this to the questions the news article says this research answers:

“How could the extreme degree of cooperation multicellular existence requires ever evolve? Why aren’t all creatures unicellular individualists determined to pass on their own genes?”2

We have here confusion between the functional grounds of a trait and the historical cause of a trait.
This presupposes that functional multicellularity evolved, and proposes that the mere existence of high-relatedness among cells is the reason why it evolved. However, creationists can also presuppose the necessity of high-relatedness among cells for functional multicellularity to be possible without an appeal to evolution.6 We have here confusion between the functional grounds of a trait and the historical cause of a trait. If multicellularity evolved, then it must have evolved from a population of clones, but this tells us very little about the succession of events that led from a unicellular ancestor to the first metazoan or plant. Therefore, it is not a helpful explanation of the evolution of multicellularity.

How useful is Dictyostelium for studying the evolution of multicellularity?

[size=10]Figure 1. Multicellular fruiting bodies ofDictyostelium discoideum.

But is Dictyostelium a model organism for studying how the evolution of multicellularity might proceed? The researchers point out that ‘cheaters’ are not a problem for Dictyostelium colonies even if they were the size of a blue whale.7 However, even the news article admits that a blue-whale-sized Dictyostelium colony is not the same thing as a blue whale.2 But it fails to describe why. It is one thing to grow a colony to the size of a blue whale, but it is a different thing to maintain the colony at that size in a multicelled state over a period of decades. The researchers admit that little cell division occurs in the multicelled phase of Dictyostelium.7 In a multicellular stage that has little cell division, there is obviously no need for strategies such as serial differentiation8 to maintain the multicelled state. Thus it is not surprising that the multicelled stage in Dictyostelium does not last very long—a day or less.
Moreover, 80% of the individual Dictyostelium cells survive the multicelled phase, and then go on to reproduce as unicellular organisms. Even volvocine algae,9 which do not possess the separation of totipotency and cellular immortality (e.g. reduced mitotic capacity or multipotency) that is the hallmark true differentiated multicellularity,10 sacrifice thousands of somatic cells in their multicellular phase to produce perhaps a dozen or so germ cells. This proportion drastically increases again out of necessity when the organism possesses a functional cellular differentiation program designed to structure and maintain the multicelled state.8 While there is an analogy to unicellular ‘bottlenecking’ in the dispersal of the spores at the end of Dictyostelium’s multicelled phase,Dictyostelium has nothing like the proportion of cellular sacrifice that occurs in multicelled life. Volvocine algae are likely the closest that life capable of free-living unicellularity can ever come to true differentiated multicellularity, and Dictyostelium doesn’t even approach this level of multicellular coordination, let alone what is found in plants, animals, and fungi. Therefore, Dictyostelium can only tell us so much about multicellular life, and it can provide little information on the historical sequence necessary to evolve true differentiated multicellularity.

Does an advantage provide an origins narrative?

Both of these studies have been said to answer some important questions about evolution. Both have been said to provide a reason why this or that trait evolved because these traits have been demonstrated to convey a certain selective advantage above the presumed ancestral condition, or the acquisition of a new trait has proved impossible without a certain feature.
The reasoning basically goes like this: “Why did x structure evolve? Because it conveyed y advantage.” There is a major fallacy here: note that this doesn’t deal with how it evolved because key causal links between the ancestral and the descendant traits have been ignored. The question of how involves discussions of evolutionary mechanisms, such as specific mutations, specific regulatory and developmental changes, their effects, and the selection mechanisms that have contributed to the preservation of these changes. Explaining the advantages of a rewired system does not explain the rewiring sequence that took place to change the old configuration into something completely new, and it does not directly explain how the wiring got there in the first place. In fact, the soundest inference from such parameters as proper wiring and fitted function is to an intentional creation, not unintentional nature.
Rarely is this sort of detailed, step-by-step narrative ever provided for even the smallest evolutionary events, let alone the massive morphological restructuring involved in turning (for example) a free-living unicellular organism into one with differentiated multicellularity, or even turning a sarcopterygian ancestor into a tetrapod descendant. On the few occasions that such plausible narratives are constructed, they are only for “incidental (and accidental) biological function”, not “essential biological structure”.11
For any fruitful debate to proceed regarding the plausibility of evolution, the right questions need to be asked and answered. Asking why one structure has an advantage over another is the wrong question with which to seek origins answers. A serious researcher would instead inquire into the feasibility of each step along a hypothetical evolutionary path, like from unicellularity to multicellularity.12 However, the science media typically obfuscates these matters, and even researchers fail to appreciate the depths of explanation that evolutionary theory needs to provide a truly compelling narrative for the history of biology capable of outweighing the design explanation with which it competes.


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 The evolution of gastrulation should be an especially important topic.

Why should we gastrulate?

Gastrulation is so familiar to us that we easily forget that its very existence is mysterious. Why do cells need to move at all? Why should the making of an animal require elaborate, origami-like folding, complex migrations and relocations? Why can’t embryos directly make the cells in their final needed place? This would certainly be possible: all major independently evolved multicellular groups (plants, fungi, and brown algae) managed to reach high levels of organization only by the use of oriented cell divisions, differential growth, and a little bit of trimming by programmed cell death. No cell migration involved, no massive tissue folding needed. Yet why does the making of all animals, from jellyfish to cockroaches to zebras, require this beautifully absurd, but universal, dance?

The historically first solution to this riddle came from the man who first recognized gastrulation (and who coined the word), the German biologist Ernst Haeckel. While Haeckel’s figure recently attracted a lot of fierce (and maybe excessive) criticisms for the inaccuracies he introduced in his drawings of embryos, he also made many seminal contributions to biology – one of which was to identify, and tentatively explain, the universal occurrence of gastrulation. His hypothesis was rooted in the early idea that embryonic development recapitulates evolution: early animals, the proposal goes, were indeed shaped as balls, even as adults, but they had the possibility to form a transient cavity by folding inwards when they touched the substrate or encountered a piece of food. The simple, temporary gut thus created allowed to locally concentrate digestive enzymes, and maybe also to trap preys. This structure was later stabilized during evolution as a permanent digestive cavity. Our own cells, Haeckel further claimed, still have to move inside during embryonic development because they recapitulate this ancestral response. By analogy to the embryonic stage (gastrula), the hypothetical ancestor was called Gastraea.

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Combinatorial Gene Control Creates Many Different Cell Types

Transcription regulators can act in combination to control the expression of an individual gene. It is also generally true that each transcription regulator in an organism contributes to the control of many genes. Combinatorial gene control makes it possible to generate a great deal of biological complexity even with relatively few transcription regulators.

Due to combinatorial control, a given transcription regulator does not necessarily have a single, simply definable function as commander of a particular battery of genes or specifier of a particular cell type. Rather, transcription regulators can be likened to the words of a language: they are used with different meanings in a variety of contexts and rarely alone; it is the well-chosen combination that conveys the information that specifies a gene regulatory event. Combinatorial gene control causes the effect of adding a new transcription regulator to a cell to depend on that cell’s past history, since it is this history that determines which transcription regulators are already present. Thus, during development, a cell can accumulate a series of transcription regulators that need not initially alter gene expression. The addition of the final members of the requisite combination of transcription regulators will complete the regulatory message, and can lead to large changes in gene expression. The importance of combinations of transcription regulators for the specification of cell types is most easily demonstrated by their ability—when expressed artificially—to convert one type of cell to another. Thus, the artificial expression of three neuron-specific transcription regulators in liver cells can convert the liver cells into functional nerve cells.

Mechanisms of Pattern Formation

A developing multicellular organism has to create a pattern in fields of cells where there was little or none before. Some of the early microscopists imagined the entire shape and structure of the human body to be already present in the sperm as a “homunculus,” a miniature human; after fertilization, the homunculus would simply grow and generate a full-sized human. We now know that this view is incorrect and that development is a progression from simple to complex, through a gradual refinement of an animal’s anatomy. To see how the whole sequence of events of spatial patterning and cell determination is set in train, we must return to the egg and the early embryo.

Different Animals Use Different Mechanisms to Establish Their Primary Axes of Polarization

Surprisingly, the earliest steps of animal development are among the most variable, even within a phylum. A frog, a chicken, and a mammal, for example, even though they develop in similar ways later, make eggs that differ radically in size and structure, and they begin their development with different sequences of cell divisions and cell specializations. Gastrulation occurs in all animal embryos, but the details of its timing, of the associated pattern of cell movements, and of the shape and size of the embryo as gastrulation proceeds are highly variable. Likewise, there is great variation in the time and manner in which the primary axes of the body become marked out. However, this polarization of the embryo usually becomes discernible very early, before gastrulation begins: it is the first step of spatial patterning. Three axes generally have to be established. The animal-vegetal (A-V) axis, in most species, defines which parts are to become internal (through the movements of gastrulation) and which are to remain external. (The bizarre name dates from a century ago and has nothing to do with vegetables.) The anteroposterior (A-P) axis specifies the locations of future head and tail. The dorsoventral (D-V) axis specifies the future back and belly. At one extreme, the egg is spherically symmetrical, and the axes only become defined during embryogenesis. The mouse comes close to being an example, with little obvious sign of polarity in the egg. Correspondingly, the blastomeres produced by the first few cell divisions seem to be all alike and are remarkably adaptable. If the early mouse embryo is split in two, a pair of identical twins can be produced— two complete, normal individuals from a single cell. Similarly, if one of the cells in a two-cell mouse embryo is destroyed by pricking it with a needle and the resulting “half-embryo” is placed in the uterus of a foster mother to develop, in many cases a perfectly normal mouse will emerge. At the opposite extreme, the structure of the egg defines the future axes of the body. This is the case for most species, including insects such as Drosophila, as we shall see shortly. Many other organisms lie between the two extremes. The egg of the frog Xenopus, for example, has a clearly defined A-V axis even before fertilization: the nucleus near the top defines the animal pole, while the mass of yolk (the embryo’s food supply, destined to be incorporated in the gut) toward the bottom defines the vegetal pole. Several types of mRNA molecules are already localized in the vegetal cytoplasm of the egg, where they produce their protein products. After fertilization, these mRNAs and proteins act in and on the cells in the lower and middle part of the embryo, giving the cells there specialized characters, both by direct effects and by stimulating the production of secreted signal proteins. For example, mRNA encoding the transcription regulator VegT is deposited at the vegetal pole during oogenesis. After fertilization, this mRNA is translated, and the resulting VegT protein activates a set of genes that code for signal proteins that induce mesoderm and endoderm, as discussed later. The D-V axis of the Xenopus embryo, by contrast, is defined through the act of fertilization. Following entry of the sperm, the outer cortex of the egg cytoplasm rotates relative to the central core of the egg, so that the animal pole of the cortex becomes slightly shifted to one side

Treatments that block the rotation allow cleavage to occur normally but produce an embryo with a central gut and no dorsal structures or D-V asymmetry. Thus, this cortical rotation is required to define the D-V axis of the future body by creating the D-V axis of the egg. The site of sperm entry that biases the direction of the cortical rotation in Xenopus, perhaps through the centrosome that the sperm brings into the egg— inasmuch as the rotation is associated with a reorganization of the microtubules nucleated from the centrosome in the egg cytoplasm. The reorganization leads to a microtubule-based transport of several cytoplasmic components, including the
mRNA coding for Wnt11, a member of the Wnt family of signal proteins, moving it toward the future dorsal side (see Figure above). This mRNA is soon translated and the Wnt11 protein secreted from cells that form in that region of the embryo activates the Wnt signaling pathway . This activation is crucial for triggering the cascade of subsequent events that will organize the dorsoventral axis of the body. (The A-P axis of the embryo will only become clear later, in the process of gastrulation.) Although different animal species use a variety of different mechanisms to specify their axes, the outcome has been relatively well conserved in evolution: head is distinguished from tail, back from belly, and gut from skin. It seems that it does not much matter what tricks the embryo uses to break the initial symmetry and set up this basic body plan.

Studies in Drosophila Have Revealed the Genetic Control Mechanisms Underlying Development

It is the fly Drosophila, more than any other organism, that has provided the key to our present understanding of how genes govern development. Decades of genetic study culminated in a large-scale genetic screen, focusing especially on the early embryo and searching for mutations that disrupt its pattern. This revealed that the key developmental genes fall into a relatively small set of functional classes defined by their mutant phenotypes. The discovery of these genes and the subsequent analysis of their functions was a famous tour de force and had a revolutionary impact on all of developmental biology, earning its discoverers a Nobel Prize. Some parts of the developmental machinery revealed in this way are conserved between flies and vertebrates, some parts not. But the logic of the experimental approach and the general strategies of genetic control that it revealed have transformed our understanding of multicellular development in general. To understand how the early developmental machinery operates in Drosophila, it is important to note a peculiarity of fly development. Like the eggs of other insects, but unlike most vertebrates, the Drosophila egg—shaped like a cucumber— begins its development with an extraordinarily rapid series of nuclear divisions without cell division, producing multiple nuclei in a common cytoplasm—a syncytium. The nuclei then migrate to the cell cortex, forming a structure called the syncytial blastoderm. After about 6000 nuclei have been produced, the plasma membrane folds inward between them and partitions them into separate cells, converting the syncytial blastoderm into the cellular blastoderm

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Experimental evolution of multicellularity 1

Multicellularity was one of the most significant innovations in the history of life, but its initial evolution remains poorly understood. Using experimental evolution, we show that key steps in this transition could have occurred quickly. We subjected the unicellular yeast Saccharomyces cerevisiae to an environment in which we expected multicellularity to be adaptive. We observed the rapid evolution of clustering genotypes that display a novel multicellular life history characterized by reproduction via multicellular propagules, a juvenile phase, and determinate growth. The multicellular clusters are uniclonal, minimizing within-cluster genetic conflicts of interest. Simple among-cell division of labor rapidly evolved. Early multicellular strains were composed of physiologically similar cells, but these subsequently evolved higher rates of programmed cell death (apoptosis), an adaptation that increases propagule production. These results show that key aspects of multicellular complexity, a subject of central importance to biology, can readily evolve from unicellular eukaryotes.

Evolution of an ancient protein function involved in organized multicellularity in animals 2

To form and maintain organized tissues, multicellular organisms orient their mitotic spindles relative to neighboring cells. A molecular complex scaffolded by the GK protein-interaction domain (GKPID) mediates spindle orientation in diverse animal taxa by linking microtubule motor proteins to a marker protein on the cell cortex localized by external cues. Here we illuminate how this complex evolved and commandeered control of spindle orientation from a more ancient mechanism. The complex was assembled through a series of molecular exploitation events, one of which – the evolution of GKPID’s capacity to bind the cortical marker protein – can be recapitulated by reintroducing a single historical substitution into the reconstructed ancestral GKPID. This change revealed and repurposed an ancient molecular surface that previously had a radically different function. We show how the physical simplicity of this binding interface enabled the evolution of a new protein function now essential to the biological complexity of many animals.

Comparative analyses have established that many protein families involved in cell adhesion, signal transduction, and cell differentiation in modern animals first appeared in the genomes of unicellular eukaryotes that were progenitors of animals (King, 2003;Nichols et al., 2006; Richter and King, 2013; Rokas, 2008). Virtually nothing is known, however, concerning the molecular mechanisms by which these proteins’ functions evolved. 


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There are three theories to discuss the mechanisms by which multicellularity could have evolved.
Symbiotic Theory - Symbitoic theory states that the first multicellular organism arose from symbiosis behaviour of different species of a single-celled organism, each performing different functions. Such symbitoic relation ship is seen between clown fish and Riterri sea anemones. 
The Cellularization Theory or The Syncytial Theory - The cellularization theory states that a unicellular organism would have developed from membrane boundaries/partitions around each nuclei from a single celled organism with multiple nuclei. Protists like ciliates and slime molds have multiple nuclei supporting this theory. 
The Colonial Theory - The colonial theory sttes that he symbiosis of many organisms of the same species led to the evolution of mutlicellular organism. This theory was proposed by Haeckel in 1874. Majority of multicellularity occurs as a consequence of the cells failing to separate following the process of division. Examples of this theory can be seen in multicellular protists like Volvox, Eudorina. 
Advantages of Multicellularity in organism are that multicellularity allows the organism to exceed the size limits. Multicelluarity also permits in increasing the complexity of the organism by allowing differentiation of numerous cellular lineages in an organism.

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Origin of metazoans

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Cell segregation and border sharpening by Eph receptor–ephrin-mediated heterotypic repulsion

The establishment of organized tissues during development requires that adjacent cell populations with distinct tissue or regional identity do not intermingle with each other. This is reflected by the formation of sharp borders between tissues or regional domains, despite the proliferation and intercalation of cells that can cause intermingling. An important mechanism to stabilize borders is to specifically restrict cells from moving between the adjacent subdivisions. Insights into mechanisms that prevent intermingling have come from experiments in which cells from different tissues are mixed in vitro, which for many cell types leads to their segregation. Such segregation occurs during development, on a more local scale, at borders that initially are fuzzy and then sharpen. Three types of mechanisms have been uncovered which can drive segregation and border formation 1

The first is differential adhesion, which has been extensively studied for cadherins that mediate homophilic cell adhesion
A second mechanism is based on increased cortical tension generated by actomyosin contraction
A third type of mechanism is cell repulsion, in which contact triggers a rapid local retraction of cell processes. For migratory cells, such repulsion is a component of the contact inhibition of locomotion, in which contact leads to a change in the direction of movement

Eph receptor tyrosine kinase and ephrin signalling has a major role in boundary formation

The relative importance of these mechanisms, and whether they are sufficient to account for cell segregation and border sharpening remain unclear.


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19 The amazing task of evolution on Tue Sep 05, 2017 7:11 am


The amazing task of evolution

The progression of biological systems: from a supposed prebiotic soup to the first self-replicating cell. From there, to the 3 domains of life: eukaryotic, archaea, and prokaryotes. From unicellular to multicellular life. From one kind of cell to specialized cells, and pluripotent cells. From there to tissues, organs, and whole bodies. From " simple " sponges to humans. EACH of these leaps of complexity is a QUANTUM step. Each node in Darwin's tree of split is the change compared to a mousetrap to a spaceship in terms of complexity. Must not EACH new cell be precisely specified through a master program which, coordinates, instructs, specifies each Cell in regard of its

1. Kind or type of cell ( Histology),
2. Cell size
3. It's specific function,
4. Position and place in the body. This is crucial. Limbs like legs, fins, eyes etc. must all be placed at the right place.  
5. How it is interconnected with other cells,
6. What communication it requires to communicate with other cells, and the setup of the communication channels
7. What specific sensory and stimuli functions are required and does it have to acquire in regard to its environment and surroundings?
8. What specific new regulatory functions it acquires
9. When will the development program of the organism express the genes to grow the new cells during development?
11. Precisely how many new cell types must be produced for each tissue and organ?
10. Specification of the cell - cell adhesion and which ones will be used in each cell to adhere to the neighbor cells ( there are 4 classes )
11. Programming of  time period the cell keeps alive in the body, and when is it time to self-destruct and be replaced by newly produced cells of the same kind
12. Set up its specific nutrition demands

I don't know how many mutations would be required in the genome to instruct all these things for one Cell. Now imagine the requirement to grow two or four legs, mutations had to generate NEW information for EACH cell, and for each new organ and body part, according to Axe's paper, 10^64 ( that's a one with 64 zeroes ) mutations for ONE positive mutation. And the information would be required in regard of body plan architecture  IN ADVANCE.  That mutation must be fixed in the genome and spread in the population. How many would be required for millions, billions of mutations to grow NEW cells, tissues, organs, and body plans? Nope, not millions, not billions, or trillions of years would be enough......  

Nah Nah.... I have not enough faith to believe in Darwin's story....

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20 Origin of cell differentiation on Thu Sep 14, 2017 10:20 am

In the scenario of a non-differentiated organism supposedly evolving into a differentiated one, the formation of new specialised cells seems to be almost as great a miracle as abiogenesis. How does the parent know what the offspring is meant to look like, and how it is to function? So according to neo-Darwinian theory, unless I am mistaken, it has to create this entirely new cell by chance, which seems quite ridiculous to me.


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Andrew Chapman wrote:In the scenario of a non-differentiated organism supposedly evolving into a differentiated one, the formation of new specialised cells seems to be almost as great a miracle as abiogenesis. How does the parent know what the offspring is meant to look like, and how it is to function? So according to neo-Darwinian theory, unless I am mistaken, it has to create this entirely new cell by chance, which seems quite ridiculous to me.


fully agreed. And the hurdles and challenge to overcome is by far greater than most proponents of evolution know of..... most are ill informed. Sadly. And so, fool themselves.

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22 Trichoplax on Fri Jun 29, 2018 6:19 pm



Trichoplax Genome Sequenced: 'Rosetta Stone' For Understanding Evolution
Molecular and evolutionary biologists have produced the full genome sequence of Trichoplax, one of nature's most primitive multicellular organisms, providing a new insight into the evolution of all higher animals. 2

As arguably the simplest free-living animals, placozoans may represent a primitive metazoan form, yet their biology is poorly understood. Here we report the sequencing and analysis of the ∼98 million base pair nuclear genome of the placozoan Trichoplax adhaerens.


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