ElShamah - Reason & Science: Defending ID and the Christian Worldview
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ElShamah - Reason & Science: Defending ID and the Christian Worldview

Otangelo Grasso: This is my library, where I collect information and present arguments developed by myself that lead, in my view, to the Christian faith, creationism, and Intelligent Design as the best explanation for the origin of the physical world.

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Why Darwin was wrong, and what really drives small adaptations ( microevolution ), and descent with modification

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Why Darwin was wrong, and what really drives descent with modification


James A. Shapiro: Evolution: A View from the 21st Century May 18, 2011
It is difficult (if not impossible) to find a genome change operator that is truly random in its action within the DNA of the cell where it works. All careful studies of mutagenesis find statistically significant non-random patterns of change, and genome sequence studies confirm distinct biases in location of different mobile genetic elements’

M.Behe:  Best of Behe: A Quick Reprise of The Edge of Evolution
Any adaptive biological feature requiring a mutational pathway of twice that complexity (that is, 4-6 mutations with the intermediate steps being deleterious) is unlikely to have arisen by Darwinian processes during the history of life on Earth.

M.Behe: Any particular adaptive biochemical feature requiring the same mutational complexity as that needed for chloroquine resistance in malaria is forbiddingly unlikely to have arisen by Darwinian processes and fixed in the population of any class of large animals (such as, say, mammals), because of the much lower population sizes and longer generation times compared to that of malaria. (By “the same mutational complexity” I mean requiring 2-3 point mutations where at least one step consists of intermediates that are deleterious, plus a modest selection coefficient of, say, 1 in 10^3 to 1 in10^4. Those factors will get you in the neighborhood of 1 in 10^20.)

An essential ingredient of Darwin's theory is that " Individuals possessing traits well suited for the struggle for local resources will contribute more offspring to the next generation ". This means that individuals with a certain genotype for a given locus or gene have more reproductive success than individuals within the same population that have other genotypes for that same gene.   What determines whether a gene variant spreads or not depends on an incredibly complex web of factors - the species' ecology, its physical and social environment and sexual behavior. A further factor adding complexity is  the fact that high social rank is associated with high levels of both copulatory behavior and the production of offspring which is widespread in the study of animal social behavior

 As alpha males have on average higher reproductive success than other males, since they outcompete weaker individuals, and get preference to copulate, if other ( weaker )  males gain beneficial mutations (or the alphas negative mutations) as the alphas can outperform and win the battle for reproduction,  thus selection has an additional hurdle to overcome and spread the new variant in the population. This does not say anything about the fact that it would have to be determined what gene loci are responsible for sexual selection and behavior, and only mutations that influence sexual behavior would have influence in fitness and the struggle to contribute more offspring to the next generation.   Science would need furthermore to have the knowledge what traits are favored in which environment. adaptation rates and mutational diversity and other spatiotemporal parameters, including population density, mutation rate, and the relative expansion speed and spatial dimensions. It is in praxis impossible to isolate these factors and see which is of selective importance,  quantify them, plug them in (usually in this context) to a mixed multivariate model, and see what's statistically significant, and get meaningful, real life results. The varying factors are too many and nonpredictive. 

In controlled circumstances, and theoretical mathematical models, evolution can be measured and calculated, but not in wild life, where the circumstances and environmental conditions change, constantly. Complex environments are unpredictable, therefore a selection process towards more complex life, even if it supposedly would exist, could not be measured.

Max. what can be said is, that theoretical, biologically realistic numerical simulations revealed that populations require inordinately long waiting times to establish even the shortest nucleotide strings. To establish a string of two nucleotides required on average 84 million years. To establish a string of five nucleotides required on average 2 billion years. We found that waiting times were reduced by higher mutation rates, stronger fitness benefits, and larger population sizes. However, even using the most generous feasible parameters settings, the waiting time required to establish any specific nucleotide string within this type of population was consistently prohibitive.


Why Darwin was wrong, and what really drives small adaptations ( microevolution ), and descent with modification Charle12

Ann Gauger the biggest problem for evolution is epistasis. And linkage decides equilibrium. Genes that are close together get dragged along with each other doing become a nation if a beneficial mutation is next to a harmful one they will rarely be separated by recombination and will tend to travel together. This means that the phenotype will be not purely selected by the beneficial mutation but rather by the combination of the two. If one of them causes the disease state then there can be linkage between whatever the beneficial trait is in the disease state. This is sometimes seen in human genetics. Second, epistasis is a major factor. Mutation can interact with one another such that they cancel each other out or have an additive effect together. This adds to the randomness of mutational process. When you add in the environmental complexity it becomes very difficult if not impossible to predict how the whole set interacts. 

I would not worry so much about sexual selection mate choice or alpha males. Those processes are the result of a global phenotype which is the sum of all these interactions I’ve mentioned. presumably, the animal with the highest fitness is the one which has the optimal combination of mutations and that would get selected by increased fitness.What this all boils down to is the problem of genotype-phenotype mapping. It is at the level of the gene that mutations occur but it is at the level of the phenotype that selection occurs.

Is there evidence for natural selection?

What we observe is gene entropy. 

1. Random mutations deteriorate the genome.
 In a new paper in Science,3Khan et al, working with Richard Lenski [Michigan State], leader of the longest-running experiment on the evolution of E. coli, found a law of diminishing returns with beneficial mutations due to negative epistasis.  The abstract said:
Epistatic interactions between mutations play a prominent role in evolutionary theories. Many studies have found that epistasis is widespread, but they have rarely considered beneficial mutations. We analyzed the effects of epistasis on fitness for the first five mutations to fix in an experimental population of Escherichia coli. Epistasis depended on the effects of the combined mutations—the larger the expected benefit, the more negative the epistatic effect. Epistasis thus tended to produce diminishing returns with genotype fitness, although interactions involving one particular mutation had the opposite effect. These data support models in which negative epistasis contributes to declining rates of adaptation over time.

2. Mechanisms that  affect the phenotype

Non random mutations: How life changes itself: the Read-Write (RW) genome 2 3

And all available scientific evidence also indicates that evolution is an engineered process. In engineering and computer science, evolution never happens by accident. It’s always the result of a deliberate act. A program that can self-evolve is always considered an engineering marvel.

The genome has traditionally been treated as a Read-Only Memory (ROM) subject to change by copying errors and accidents. 7  I propose that we need to change that perspective and understand the genome as an intricately formatted Read-Write (RW) data storage system constantly subject to cellular modifications and inscriptions. Cells operate under changing conditions and are continually modifying themselves by genome inscriptions. These inscriptions occur over three distinct time-scales (cell reproduction, multicellular development, and evolutionary change) and involve a variety of different processes at each time scale (forming nucleoprotein complexes, epigenetic formatting and changes in DNA sequence structure). Research dating back to the 1930s has shown that genetic change is the result of cell-mediated processes, not simply accidents or damage to the DNA. This cell-active view of genome change applies to all scales of DNA sequence variation, from point mutations to large-scale genome rearrangements and whole genome duplications (WGDs). This conceptual change to active cell inscriptions controlling RW genome functions has profound implications for all areas of the life sciences.

Ever since the formulation of the neo-Darwinist Modern Synthesis evolutionary theoryin the 1930s and 1940s, it has been an article of faith that hereditary variation results from stochastic copying errors and unavoidable damage to the genome

In the past 60 years, since the structure of DNA was elucidated, molecular biologists have studied the basic mechanisms of long-term genome change. They have discovered a wide array of proofreading and damage repair biochemical systems that remove copying errors and correct DNA damage. At the same time, they have revealed an amazing and wholly unanticipated array of cellular and molecular systems that operate to generate genome variability, both temporary and structural. As we begin the second decade of the 21st century, accumulating empirical evidence has thus shifted the perspective on genome variation to that of an active inscription process changing the information passed on to future generations.


Additional phenomena, such as developmental modules, entrenchment, and robustness, further separate random mutations at the DNA level from expressed phenotypes at the level of organisms.
The different components of a genome and/or of a developmental structure usually have different effects 'downstream', that is, on the characteristics of the fully developed adult, through the entire lifetime. The magnitude of these effects is measured by the 'entrenchment' of that structure. The entrenchment of a gene or a gene complex changes by degrees - it's not an all-or-none property. From an evolutionary point of view, the entrenchment of a unit has multiple and deep consequences for its role in different groups of organisms and different species, notably affecting other units that depend on its functioning. Generative entrenchment is seen both as an 'engine' of development and evolutionary change and as a constraint. This amounts to saying that crucial developmental factors ('pivots' in Wimsatt's terms) may be highly conserved and be buffered against change, or may undergo minor heritable changes with major evolutionary consequences. Generative entrenchment, as the expression aptly suggests, is very probably linked to spontaneous and quite general collective form-generating processes, but it is (of course) also under the control of genes, gene complexes, and developmental pathways. How these different sources of order and change (some generically Physico-chemical and some specifically genetic) interact is still largely unknown.

A trait is said to be robust with respect to a genetic or environmental variable if variation of the one is only weakly correlated with variations in the other. In other words, robustness is the persistence of a trait of an organism under perturbations, be they random developmental noise, environmental change or genetic change. In recent years, robustness has been shown to be of paramount importance in understanding evolution, because robustness permits hidden genetic variation to accumulate. Such hidden variation may serve as a source of new adaptations and evolutionary innovations.  It is an open, empirical and highly substantive question how narrowly such endogenous effects constrain the phenotypic variations on which external selection operates. It will take a while to find out. But, until that question gets answered, it is unadvisable to take a neo-Darwinist account of evolution for granted.

Master genes are 'masters'
Many different traits are indissociably genetically controlled by the same 'master gene'. Any mutation affecting one master gene, if viable, has an impact on many traits at once.  A well studied gene family, called Otx, masterminds the development of kidneys, cranio-facial structures (Suda et al., 2009), gutsgonads and the cerebral cortex (segmentation and cortical organization). 

Developmental modules
Let's start with a definition. A module is a unit that is highly integrated internally and relatively insensitive to context externally. Developmental modules exist at different levels of the organization, from gene regulation to networks of interacting genes to organ primordia. They are relatively insensitive to the surrounding context and can thus behave invariantly, even when they are multiply realized in different tissues and in different developmental phases. Different combinations of developmental modules in each context, however, produce a difference in their functions in development. There is evidence of the integration of several interacting elements into a module when perturbation of one element results in perturbations of the other elements in that module, or in gene-gene interaction (epistasis) within the module, in such a way that the overall developmental input-output relation is altered. This is another signal case in which the conservation of genetic and developmental building blocks, together with their multiple recombinations in different tissues and organisms, explains the diversity of life forms as well as the invariance of basic body plans.  The reverberation of the effects of gene mutations is usually multiple and only the viable overall result is then accessible to selection. This complex system of master signals regulates tissues as different as the central nervous system, pharynx, hair cells, odontoblasts, kidney, feathers, gut, lung, pancreas, hair and ciliated epidermal cells across many different vertebrate and invertebrate species. Every mutation in any one of the genes involved will alter many organs and their functions - a far cry from 'beanbag genetics'. The lesson here is that modularity gives a new complex picture of evolution, one in which internal constraints and internal dynamics filter what selection can act upon, and to what extent it can do so. Precisely because so much cannot change, other things can change at the (so to speak) genetic periphery of organisms. It is often (although not always) the case that when we witness gene duplications, a ubiquitous kind of genetic modification, the 'original' gene continues acting as it did in earlier forms of life, while the 'copy' can 'explore' new functions over evolutionary time (these metaphors are commonplace in the professional literature) .

The Russian zoologist and evolutionist Ivan Ivanovich Schmalhausen (1884-1963) had rightly stressed that living organisms are not the mere atomic 'a position' of separate parts, but rather highly 'coordinated' systems (for a historical and critical review, see Levit et al., 2006). Today justice is done to Schmalhausen by experimental evidence that some mutations in genes specifically affecting one part of the body carry with them suitable modifications in other related parts. When limbs are induced ectopically (that is, where they don't belong), often sensory neurons, receptor organs, cartilage and blood vessels also develop as a consequence around them (see Kirschner and Gerhart, 2005 for stunning examples). A laboratory-induced and quantitatively controllable modification in two key proteins in chick and finch embryos early in development produces as the main result variable elongation

Tomi Aalto

1. RNA methylation
2. DNA dinucleotide methylation
3. DNA CpG island methylation
4. Histone methylation
5. Chromatin remodeling
6. DNA coiling
7. MicroRNA regulation
8. Alternative splicing
9. Flanking binding sites of the DNA

No gene sequence alterations in the list, because
- Deletions, insertions and frameshift mutations during protein synthesis are misinterpretations of the alternative splicing mechanism
- Retrogenes and genetic recombinations are misinterpretations of microRNAs and the alternative splicing mechanism
- RNA based gene duplications are misinterpretations of the alternative splicing mechanism

So, what do the evolutionists have for supporting their idea of random mutations and natural selection?

Point mutations, which don't occur randomly. Methylated cytosine may flip to thymine and this alteration will not be repaired by the repair mechanisms. This is a designed feature. Hydroxymethylated cytosine turns to Guanine and this seems to be another epigenetic-based mechanism. The immune system is a dynamic part of the genome and some genes may be altered due to defense mechanism against pathogens.

1.The alternative role of DNA methylation in splicing regulation

2. Co-regulation of miRNA biogenesis and alternative pre-mRNA splicing of host gene

3. Histone methylation, alternative splicing, and neuronal differentiation.

Seven things Darwin didn't tell you because he didn't know.
1. Alterations in diet, climate, stress and other environmental factors cause mechanism based inheritable changes in organisms, not random mutations and selection.
An example: Italian wall lizards experienced radical changes in morphology and behavior after changing their diet from insects to plants. This occurred very rapidly, just in three decades. They even had a 'new' structure in their gut, so called Cecal Valve. Genes that control the growth of the Cecal Valve were differently expressed due to the changed diet.
2. Random mutations don't enhance the genomic information. Random mutations are genetic errors and they destroy biological information and disrupt genetic integrity.
An example: There are about 200,000 disease-causing genetic mutations in the human DNA pointing out that evolution is not happening and that so called natural selection is not able to weed those mutations out.
3. Most of so-called mutations are not random changes. Genetic changes occur due to oxidative stress, changing diet, exposure to toxins, disrupted methylation patterns, viruses etc. However, most of them still disrupt genetic integrity.
- A lack of methyl groups in gene body may develop cancer and trigger genetic mutations.
- Viruses play a potential role in causing aberrant methylation patterns. According to a fresh study, more than 1 in 5 adults has cancer-causing HPV infection.
4. Biological information is multi-layered. There are at least three forms of biological information in the cell:
1. Gene sequences - Digital information layer
2. Epigenetic markers, 3D genome, flanking binding sites - Analog information layer
3. Gene regulatory networks, genomic integrity and stability - Meta data
- The cell uses cytokines as knobs instead of switches.
- DNA methylation influences continuous variation in ant worker size
5. Biological information is extremely complex. The 'grammar' of the human genetic code is more complex than that of even the most intricately constructed spoken languages in the world.
6. Organisms can experience rapid variation due to epigenetic mechanisms.
7. Life is not driven by gene sequences. Genes are driven by lifestyle.

The industrial melanism mutation in British peppered moths is a transposable element. 5
Discovering the mutational events that fuel adaptation to environmental change remains an important challenge for evolutionary biology. The classroom example of a visible evolutionary response is industrial melanism in the peppered moth (Biston betularia): the replacement, during the Industrial Revolution, of the common pale typica form by a previously unknown black (carbonaria) form, driven by the interaction between bird predation and coal pollution. The carbonaria locus has been coarsely localized to a 200-kilobase region, but the specific identity and nature of the sequence difference controlling the carbonaria-typica polymorphism, and the gene it influences, are unknown. Here we show that the mutation event giving rise to industrial melanism in Britain was the insertion of a large, tandemly repeated, transposable element into the first intron of the gene cortex. Statistical inference based on the distribution of recombined carbonaria haplotypes indicates that this transposition event occurred around 1819, consistent with the historical record. We have begun to dissect the mode of action of the carbonaria transposable element by showing that it increases the abundance of a cortex transcript, the protein product of which plays an important role in cell-cycle regulation, during early wing disc development. Our findings fill a substantial knowledge gap in the iconic example of microevolutionary change, adding a further layer of insight into the mechanism of adaptation in response to natural selection. The discovery that the mutation itself is a transposable element will stimulate further debate about the importance of 'jumping genes' as a source of major phenotypic novelty.

Moving through the Stressed Genome: Emerging Regulatory Roles for Transposons in Plant Stress Response 6
The recognition of a positive correlation between organism genome size with its transposable element (TE) content, represents a key discovery of the field of genome biology. Considerable evidence accumulated since then suggests the involvement of TEs in genome structure, evolution and function. The global genome reorganization brought about by transposon activity might play an adaptive/regulatory role in the host response to environmental challenges, reminiscent of McClintock's original ‘Controlling Element’ hypothesis. This regulatory aspect of TEs is also garnering support in light of the recent evidences, which project TEs as “distributed genomic control modules.” According to this view, TEs are capable of actively reprogramming host genes circuits and ultimately fine-tuning the host response to specific environmental stimuli. Moreover, the stress-induced changes in epigenetic status of TE activity may allow TEs to propagate their stress responsive elements to host genes; the resulting genome fluidity can permit phenotypic plasticity and adaptation to stress. Given their predominating presence in the plant genomes, nested organization in the genic regions and potential regulatory role in stress response, TEs hold unexplored potential for crop improvement programs. This review intends to present the current information about the roles played by TEs in plant genome organization, evolution, and function and highlight the regulatory mechanisms in plant stress responses. We will also briefly discuss the connection between TE activity, host epigenetic response and phenotypic plasticity as a critical link for traversing the translational bridge from a purely basic study of TEs, to the applied field of stress adaptation and crop improvement. TEs not only rewire host transcriptional circuits in times of stress, but the extensive genomic rearrangements mediated by such TE bursts shapes genome architecture, ultimately leading to speciation and evolution of plant genomes.  

Profuse evolutionary diversification and speciation on volcanic islands: transposon instability and amplification bursts explain the genetic paradox 1
Eukaryotic genomes harbor many families of transposable elements (TEs) that are mobilized by genome shock; these elements may be the primary drivers of genetic reorganization and speciation on volcanic islands.   TEs are a key factor, even a prerequisite, in the evolution of species-rich lineages. Thus evolutionarily constrained lineages may be unable to undergo the rapid genome remodeling that leads to an adaptive radiation primarily because of a severe lack of TEs in their ancestral genomes. On the other hand, lineages with abundant TEs in their genomes are equipped to respond to the stress of founder events and the harsh conditions of active volcanic habitats by generating a host of new genetic combinations as a result of bursts of TE amplification, setting the stage for profuse speciation and adaptive radiation. TEs may therefore play a critical role in the survival, rampant speciation and adaptation of plants and animals in volcanic environments, and may underlie many of the evolutionary innovations frequently associated with adaptive radiations.

Fungal evolutionary genomics provides insight into the mechanisms of adaptive divergence in eukaryotes 2
Many predictions have been validated, such as the role of gene duplication in novel functions, the positive impact of TEs on evolvability, the importance of changes in gene regulation, the clustering of some adaptive changes in particular genomic regions and the occurrence of BDM incompatibilities 3. Other processes, previously considered anecdotal, have been shown to feature prominently among the drivers of adaptive divergence. These processes include gene deletions, introgressions, changes in genomic architecture and HGTs. The strength and nature of ecologically based divergent selection or life cycle characteristics have also been shown to be important. The genomic heterogeneity in rates of evolution in some fungi, with regions differing in their susceptibility to mutations, may facilitate the resolution of an apparent ‘conflict of interest’ between different classes of genes. Isochore-like structures, for instance, make it possible to cope with trade-offs in which there is a need to maintain some functions under strong constraints, with others evolving rapidly in response to positive selection. This trade-off may also be resolved by gene regulation, with promoters differing in evolvability according to the type of function.

Adaptation to Global Change: A Transposable Element–Epigenetics Perspective  4
Understanding how organisms cope with global change is a major scientific challenge. The molecular pathways underlying rapid adaptive phenotypic responses to global change remain poorly understood. Here, we highlight the relevance of two environment-sensitive molecular elements: transposable elements (TEs) and epigenetic components (ECs).

Transposable element islands facilitate adaptation to novel environments in an invasive species 4
Adaptation requires genetic variation, but founder populations are generally genetically depleted. Here we sequence two populations of an inbred ant that diverge in phenotype to determine how variability is generated. Cardiocondyla obscurior has the smallest of the sequenced ant genomes and its structure suggests a fundamental role of transposable elements (TEs) in adaptive evolution. Accumulations of TEs (TE islands) comprising 7.18% of the genome evolve faster than other regions with regard to single-nucleotide variants, gene/exon duplications and deletions and gene homology. A non-random distribution of gene families, larvae/adult specific gene expression and signs of differential methylation in TE islands indicate intragenomic differences in regulation, evolutionary rates and coalescent effective population size. Our study reveals a tripartite interplay between TEs, life history and adaptation in an invasive species. Mechanisms controlling TEs are as old as prokaryotes9 and in fact most TEs are epigenetically silenced  through either methylation, histone modifications or RNAi   The current understanding of TE activity dynamics in genomes is that periods of relative dormancy are followed by bursts of activity, often induced by biotic and abiotic stress, such as exposure to novel habitats. Frequent TE transposition during bursts leads to genomic rearrangements, thus producing new genetic variants and eventually even promoting speciation TEs represent a major force in evolution, contributing to the generation of genetic variation especially in species confronted with hurdles like inbreeding or repeated bottlenecks.

Friend or Foe: Epigenetic Regulation of Retrotransposons in Mammalian Oogenesis and Early Development 7
TEs bridge genetic and epigenetic landscapes because TEs are genetic elements whose silencing and de-repression are regulated by epigenetic mechanisms that are sensitive to environmental factors. Ultimately, transposition events can change size, content, and function of mammalian genomes. Thus, TEs act beyond mutagenic agents reshuffling the genomes, and epigenetic regulation of TEs may act as a proximate mechanism by which evolutionary forces increase a species’ hidden reserve of epigenetic and phenotypic variability facilitating the adaptation of genomes to their environment.  If we put aside the mechanistic details of precise molecular interactions, it seems that epigenetic regulation of TEs may act as a proximate mechanism by which evolutionary forces, and selection pressure, utilize TEs to increase the species’ “hidden reserve of variability”

Plants’ Epigenetic Secrets

While the mechanisms that determine biodiversity , bodyshape, phenotype and primary speciation  were pretty clear to me after my  investigations, and  the evidence that came to light provided good reasons to refute darwinian  macro-evolution as possible mechanism,

Where Do Complex Organisms Come From?

it was not really elucidated  what mechanisms determine adaptation to the environment, and microevolution. I knew it was a pre-programmed process, based on the work of Shapiro, McClintock et al, and proponents of the third way


Only who has no grasp whatsoever about how evolution works, can believe, that microevolution can lead to macroevolution and biodiversity.  I have not found any scientific paper that provided conclusive proof and evidence  that mutations , natural selection or genetic drift  provide organismal  adaptation to stress , ecological niches and separation, and microevolution, or even macro-evolution. But papers that refute the claim :

The frailty of adaptive hypotheses for the origins of organismal complexity
There is no evidence at any level of biological organization that natural selection is a directional force encouraging complexity. 

The evidence also refutes  the hypothesis of macroevolution 

Macroevolution. Fact, or fantasy ?

I read already about Transposons and their various essential functions :

Transposons and Retrotransposons

but today came the aha! breakthrough moment. After googling, i found the papers that made it clear that transposable elements  (TE's) , which were called junk , play a major if not the main role in microevolution, and so do epigenetic gene regulatory networks that orchestrate TE's responsible for the adaptation of organisms, and their species restricted physical change.

Stephen C. Meyer, Darwin's doubt, page 167:
Evolutionary scenarios envisioning other mutational mechanisms also presuppose important sources of preexistent genetic information. Gene duplication, as the name implies, involves the production of a duplicate copy of a preexisting gene, already rich in functionally specified information. Retropositioning of messenger RNA transcripts occurs when an enzyme called reverse transcriptase takes a preexisting strand of messenger RNA and inserts its corresponding DNA sequence into a genome, also producing a duplicate of the coding portion of a preexisting gene. Lateral gene transfer involves transferring a preexisting gene from one organism (usually a bacterium) into the genome of another. The transfer of mobile genetic elements likewise occurs when preexisting genes enclosed in circular strands of DNA called plasmids enter one organism from another and eventually find themselves incorporated into a new genome. This process also mainly occurs in single-celled organisms. A similar process can occur in eukaryotes, where mobile genetic elements called transposons—often called “jumping genes”—can hop from place to place in the genome. Gene fusion occurs when two adjacent preexisting genes, each rich with specified genetic information, link together after the deletion of intervening genetic material.” Each of these six mutational mechanisms presupposes preexisting modules of specified genetic information. Some of these mutational mechanisms also depend upon sophisticated preexistent molecular machines such as the reverse transcriptase enzyme used in retropositioning or other complex cellular machinery involved in DNA replication. Since building these machines requires other sources of genetic information, scenarios that presuppose the availability of such molecular machines to assist in the cutting, splicing, or positioning of modular sections of genetic information clearly beg the question.

Behe, McKenzie-Discovery lecture


Please provide evidence of differential reproduction, how it was measured in a natural environment, where the circumstances and environmental conditions change, constantly, and the results published in a peer reviewed scientific journal. And how a uniform model of genomic change was generated which indicates that differential reproduction happens due to natural selection, drift, and gene flow.

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5012101/[/url
2. https://hal.archives-ouvertes.fr/hal-01302695/document
3. http://rstb.royalsocietypublishing.org/content/365/1547/1825
4. http://www.nature.com/articles/ncomms6495
5. https://www.ncbi.nlm.nih.gov/pubmed/27251284
6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5056178/
7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5168827/

Further readings :

How Junk DNA confirms intelligent design predictions

But, But, But … We’re 98% Similar to the Chimp!

Last edited by Otangelo on Mon Jun 21, 2021 7:01 am; edited 22 times in total




Macroevolution. Fact, or fantasy? 


Microevolution and secondary speciation is a fact. The macro change however from one organism into another in long periods of time, the change of body plans and evolutionary novelties, phenotypic complexity and phenotypic novelty is not a fact, not even a theory, or even a hypothesis. It's just fantasy without a shred of evidence. It's not possible.  Show me some examples of observed facts;  please provide and give me empirical data of a unorganized undirected unguided Neo-Darwinian accidental random macroevolutionary event of a change/transition, where  one "kind" can evolve into another beyond the species level (i.e. speciation) ,  like a organism randomly changing/transition into a whole entire different, new fully functioning biological features in an organism, the emergence of new complex functions, a new genus or higher rank in taxonomy, with the rise of new body plans, What is an evolutionary novelty? A list of most-often cited examples include the shell of turtles (Cebra-Thomas et al. 2005), flight (Prum 2005), flowers (Albert, Oppenheimer, and Lindqvist 2002), the ability of great tits to open bottles of milk (Kothbauerhellmann 1990), the transition from the jaw to the ear of some bones during the evolution of mammals from reptiles (Brazeau and Ahlberg 2006), eyes (Fernald 2006), hearts (Olson 2006), bipedalism (Richmond and Strait 2000), and the origin of Hox genes (Wagner, Amemiya, and Ruddle 2003);   Ernst Mayr, a major figure of the MS, defined novelties as “any newly acquired structure or property that permits the performance of a new function, which, in turn, will open a new adaptive zone” (Mayr 1963, 602)something that we merely don't have to just put  blind faith in?

Where Do Complex Organisms Come From?


Cell and body shape, and organism development does NOT depend exclusively on genetic information.

Stephen C. Meyer, Darwin's doubt: 

These different sources of epigenetic information in embryonic cells pose an enormous challenge to the sufficiency of the neo-Darwinian mechanism. According to neo-Darwinism, new information, form, and structure arise from natural selection acting on random mutations arising at a very low level within the biological hierarchy—within the genetic text. Yet both body-plan formation during embryological development and major morphological innovation during the history of life depend upon a specificity of arrangement at a much higher level of the organizational hierarchy, a level that DNA alone does not determine. If DNA isn’t wholly responsible for the way an embryo develops— for body-plan morphogenesis—then DNA sequences can mutate indefinitely and still not produce a new body plan, regardless of the amount of time and the number of mutational trials available to the evolutionary process. Genetic mutations are simply the wrong tool for the job at hand. Even in a best-case scenario—one that ignores the immense improbability of generating new genes by mutation and selection—mutations in DNA sequence would merely produce new genetic information. But building a new body plan requires more than just genetic information. It requires both genetic and epigenetic information—information by definition that is not stored in DNA and thus cannot be generated by mutations to the DNA. It follows that the mechanism of natural selection acting on random mutations in DNA cannot by itself generate novel body plans, such as those that first arose in the Cambrian explosion.

Centrosomes play a central role in development: a frog egg can be induced to develop into a frog merely by injecting a sperm centrosome—no sperm DNA is needed. Another non-genetic factor involved in development is the membrane pattern of the egg cell. 

Organismal form and function depend upon the precise arrangement of various constituents as they arise during, or contribute to, embryological development. Thus, the specific arrangement of the other building blocks of biological form—cells, clusters of similar cell types, dGRNs, tissues, and organs—also represent a kind of specified or functional information.

genes alone do not determine the three-dimensional form and structure of an animal.  Developmental biologists, in particular, are now discovering more and more ways that crucial information for building body plans is imparted by the form and structure of embryonic cells, including information from both the unfertilized and fertilized egg. DNA helps direct protein synthesis. Parts of the DNA molecule also help to regulate the timing and expression of genetic information and the synthesis of various proteins within cells. Yet once proteins are synthesized, they must be arranged into higher-level systems of proteins and structures.
The three-dimensional structure or spatial architecture of embryonic cells plays important roles in determining body-plan formation during embryogenesis. Developmental biologists have identified several sources of epigenetic information in these cells.

The precise arrangement of microtubules in the cytoskeleton constitutes a form of critical structural information. neither the tubulin subunits, nor the genes that produce them, account for the differences in the shape of the microtubule arrays that distinguish different kinds of embryos and developmental pathways. Instead, the structure of the microtubule array itself is, once again, determined by the location and arrangement of its subunits, not the properties of the subunits themselves. Jonathan Wells explains it this way: “What matters in [embryological] development is the shape and location of microtubule arrays, and the shape and location of a microtubule array is not determined by its units.” Directed transport involves the cytoskeleton, but it also depends on spatially localized targets in the membrane that are in place before transport occurs. Developmental biologists have shown that these membrane patterns play a crucial role in the embryological development of fruit flies.

Membrane Targets
Preexisting membrane targets, already positioned on the inside surface of the egg cell, determine where these molecules will attach and how they will function. These membrane targets provide crucial information—spatial coordinates—for embryological development.

Ion Channels and Electromagnetic Fields
Experiments have shown that electromagnetic fields have “morphogenetic” effects—in other words, effects that influence the form of a developing organism. In particular, some experiments have shown that the targeted disturbance of these electric fields disrupts normal development in ways that suggest the fields are controlling morphogenesis.2 Artificially applied electric fields can induce and guide cell migration. There is also evidence that direct current can affect gene expression, meaning internally generated electric fields can provide spatial coordinates that guide embryogenesis.3 Although the ion channels that generate the fields consist of proteins that may be encoded by DNA (just as microtubules consist of subunits encoded by DNA), their pattern in the membrane is not. Thus, in addition to the information in DNA that encodes morphogenetic proteins, the spatial arrangement and distribution of these ion channels influences the development of the animal.

The Sugar Code
These sequence-specific information-rich structures influence the arrangement of different cell types during embryological development. Thus, some cell biologists now refer to the arrangements of sugar molecules as the “sugar code” and compare these sequences to the digitally encoded information stored in DNA. As biochemist Hans-Joachim Gabius notes, sugars provide a system with “high-density coding” that is “essential to allow cells to communicate efficiently and swiftly through complex surface interactions.” According to Gabius, “These [sugar] molecules surpass amino acids and nucleotides by far in information-storing capacity.” So the precisely arranged sugar molecules on the surface of cells clearly represent another source of information independent of that stored in DNA base sequences.  These cascades are, along with the cell event itself, associated with the “coding information” on a cell surface, or, using another terminology, are realized due to an instruction for the cell from the morphogenetic field of an organism. The concrete signal transduction pathways connecting the "coding information" on a cell surface and the expression of the given sets of genes need to be elucidated. 

Meyer, Darwins doubt, page 212:

According to neo-Darwinism, new information, form, and structure arise from natural selection acting on random mutations arising at a very low level within the biological hierarchy—within the genetic text. Yet both body-plan formation during embryological development and major morphological innovation during the history of life depend upon a specificity of arrangement at a much higher level of the organizational hierarchy, a level that DNA alone does not determine. If DNA isn’t wholly responsible for the way an embryo develops— for body-plan morphogenesis—then DNA sequences can mutate indefinitely and still not produce a new body plan, regardless of the amount of time and the number of mutational trials available to the evolutionary process. Genetic mutations are simply the wrong tool for the job at hand.

Even in a best-case scenario—one that ignores the immense improbability of generating new genes by mutation and selection—mutations in DNA sequence would merely produce new genetic information. But building a new body plan requires more than just genetic information. It requires both genetic and epigenetic information—information by definition that is not stored in DNA and thus cannot be generated by mutations to the DNA. It follows that the mechanism of natural selection acting on random mutations in DNA cannot by itself generate novel body plans, such as those that first arose in the Cambrian explosion.

Cell and body shape, and organism development depends on following : 

Membrane targets and patterns 
Cytoskeletal arrays

Ion channels, and 
Sugar molecules on the exterior of cells (the sugar code)

Gene regulatory networks

Various codes and the encoded epigenetic information is required:

The Genetic Code 
The Splicing Codes
The Metabolic Code
The Signal Transduction Codes 
The Signal Integration Codes 
The Histone Code 
The Tubulin Code
The Sugar Code 
The Glycomic Code
The calcium Code
The RNA Code

" Junk DNA "

MicroRNAs--"Once Dismissed as Junk"--Confirmed To Have Important Gene Regulatory Function

In 2008 Scientific American noted that microRNAs were "once dismissed as junk" and said the following:
Tiny snippets of the genome known as microRNA were long thought to be genomic refuse because they were transcribed from so-called "junk DNA," sections of the genome that do not carry information for making proteins responsible for various cellular functions. Evidence has been building since 1993, however, that microRNA is anything but genetic bric-a-brac. Quite the contrary, scientists say that it actually plays a crucial role in switching protein-coding genes on or off and regulating the amount of protein those genes produce.

Transposons and Retrotransposons

striking evidence has accumulated indicating that some proviral sequences and HERV proteins might even serve the needs of the host and are therefore under positive selection. The remarkable progress in the analysis of host genomes has brought to light the significant impact of HERVs and other retroelements on genetic variation, genome evolution, and gene regulation.

Principal Meanings of Evolution in Biology Textbooks 1

What is fact :
1. Change over time; history of nature; any sequence of events in nature
2. Changes in the frequencies of alleles in the gene pool of a population
3. Limited common descent: the idea that particular groups of organisms have descended from
a common ancestor.
4. The mechanisms responsible for the change required to produce limited descent with modification; chiefly natural selection acting on random variations or mutations

What is not fact: 
5. Universal common descent: the idea that all organisms have descended from a single common ancestor.
6. Blind watchmaker thesis: the idea that all organisms have descended from common ancestors through unguided, unintelligent, purposeless, material processes such as natural
selection acting on random variations or mutations; the idea that the Darwinian mechanism of natural selection acting on random variation, and other similarly naturalistic mechanisms, completely suffice to explain the origin of novel biological forms and the appearance of design in complex organisms.




How genetic mutations affect development more complex than previously thought

Excerpt: "A large-scale study, published in Wellcome Open Research and which passed peer review today, has shown that inactivating the same gene in mouse embryos that are virtually genetically identical can result in a wide range of different physical features or abnormalities. This suggests that the relationship between gene mutation and consequence is more complex than previously suspected.
The researchers, from the Deciphering the Mechanisms of Development Disorders (DMDD) consortium that is coordinated at the Francis Crick Institute, looked at 220 mouse embryos each missing one of 42 different genes. By scanning the entire embryo in minute detail, the researchers picked up on even the smallest differences in features – right down to the level of whether the structure of individual nerves, muscles and small blood vessels were abnormal.
The genes studied by DMDD are known as ‘embryonic lethal’, because they are so crucial to development that an embryo missing any one of them can’t survive to birth. Studying these genes can help us understand how embryos develop, why some miscarry, and why some mutations can lead to abnormalities at birth.
Clinicians commonly find that people with the same genetic disease can show different symptoms or be affected with differing severity. In part this is likely to be due to the fact that we all differ in our precise genetic makeup. However, this study in mice shows that even when individuals have virtually identical genomes, the same mutation can lead to a variety of different outcomes amongst affected embryos.
“This is a striking result, coming as it does from such a large study in which embryos have been studied in unprecedented detail. It shows us that even with an apparently simple and well-defined mutation, the precise outcome can be both complex and variable. We have a lot to learn about the roles of these lethal genes in embryonic development to understand why this happens.
“This is a surprising result, and more research into gene function is needed in order to make sense of the finding.”
(Dr Tim Mohun, who led the study at Deciphering the Mechanisms of Developmental Disorders (DMDD))"
My comment: They didn't take into account the several forms of biological information. And they didn't take into account that control of embryonic cell development is not guided by genes inside the embryo, but several epigenetic mechanisms outside the embryo.
When they can't prove that whole gene knockouts affect certain traits, then how come could they prove that small point mutations affect certain traits? This is why all claims regarding point mutations induced gene alleles and their assumed impact on traits are now questioned.
Darwinists have a serious Missing Heritability problem. Life is not driven by gene sequences. Genes are driven by lifestyle. The evolutionary theory is a major heresy. Don't get misled.




Adaptation of cells to new environments


Several life-essential EPIGENETIC mechanisms respond to environmental stress. 

- heat shock factors (HSFs)
- The unfolded protein response (UPR)
- nonhomologous end-joining and homologous recombination
- The DNA Damage Response
- The Response to Oxidative Stress

Evolution takes supposedly thousands of years to gain an environmental advantage. So what environmental benefit would evolution supposedly provide, if adapting and responding to environmental stimuli is not only a life-essential process which had to be fully implemented when life began but, furthermore, a pre-programmed process based on information through signaling networks?

Cells have many mechanisms to modulate the signaling pathways at transcriptional, post-transcriptional and post-translational levels.

Organisms respond to short-term environmental changes by reversibly adjusting their physiology to maximize resource utilization while maintaining structural and genetic integrity by repairing and minimizing damage to cellular infrastructure, thereby balancing innovation with robustness. The cell’s initial response to a stressful stimulus is geared towards helping the cell to defend against and recover from the insult. 2 The fact that the cell’s survival critically depends on the ability to mount an appropriate response towards environmental or intracellular stress stimuli can explain why this reaction is highly conserved in evolution. The adaptive capacity of a cell ultimately determines its fate.

One of the reasons behind the evolutionary success of mammals (and other multicellular organisms) is their extraordinary capacity to adapt to changing environmental conditions. 3

Maybe the author should ask himself, how the Cell could have survived without the mechanism implemented from day one !!

If the stress stimulus does not go beyond a certain threshold, the cell can cope with it by mounting an appropriate protective cellular response, which ensures the cell’s survival. One of the main prosurvival activities of cells, the heat shock response, was originally described as the biochemical response of cells to mild heat stress (i.e., elevations in temperature of C above normal) During initiation of the heat shock response general protein transcription and translation is halted, presumably to alleviate the burden of misfolded proteins in the cell. However, transcription factors that enhance expression of a specific subset of protective genes are selectively activated under these conditions; these are the heat shock factors (HSFs) Vertebrate cells have three different HSFs: HSF1 is essential for the heat shock response and is also required for developmental processes, HSF2 and HSF4 are important for differentiation and development, while HSF3 is only found in avian cells and is probably redundant with HSF1 .

Secretory and membrane proteins undergo posttranslational processing, including glycosylation, disulfide bond formation, correct folding, and oligomerization, in the ER. In order to effectively produce and secrete mature proteins, cellular mechanisms for monitoring the ER environment are essential. Exposure of cells to conditions such as glucose starvation, inhibition of protein glycosylation, disturbance of Ca2+ homeostasis and oxygen deprivation causes accumulation of unfolded proteins in the ER (ER stress) and results in the activation of a well-orchestrated set of pathways during a phenomenon known as the unfolded protein response (UPR)

Upon cellular stress conditions that are caused by exposure to chemotherapeutic agents, irradiation, or environmental genotoxic agents such as polycyclic hydrocarbons or ultraviolet (UV) light, damage to DNA is a common initial event DNA double-strand breaks (DSBs) and single-strand breaks (SSBs) are considered as key lesions that initiate the activation of the DNA damage response. Damage to DNA engages DNA repair processes to ensure the cell’s survival in the case of sublethal damage. Depending on the type of lesion, DNA damage initiates one of several mammalian DNA repair pathways, which eventually restore the continuity of the DNA double strand. There are two main pathways for the repair of DSBs, that is, nonhomologous end-joining and homologous recombination

Cell survival requires appropriate proportions of molecular oxygen and various antioxidants. Reactive products of oxygen are amongst the most potent and omnipresent threats faced by cells. These include ROS such as

superoxide anion
hydrogen peroxide (H2O2)
singlet oxygen
hydroxyl radical (OH•)
peroxy radicals
the second messenger nitric oxide (NO•) which can react with O2 to form peroxynitrite (ONOO−)

Infectious agents can drive a plethora of stress responses by activating pattern recognition receptors. In the initiation of innate immune responses against pathogens, pattern-recognition receptors (PRRs) have an essential role in recognizing specific components of microorganisms and triggering responses that eliminate the invading microorganisms. However, inappropriate activation of PRRs can lead to prolonged inflammation and even to autoimmune and inflammatory diseases. Thus, PRR-triggered responses are regulated through the degradation or translocation of the innate receptors themselves and through the involvement of intracellular regulators or amplifiers. In addition, a complex interplay between PRRs and/or other immune pathways finely tunes the outcome of host immune defense responses. 4

Considerable evidence has now accumulated indicating that the intracellular mechanisms that are activated in response to different stresses — which include the DNA damage response, the unfolded protein response, mitochondrial stress signalling and autophagy — as well as the mechanisms ensuring the proliferative inactivation or elimination of terminally damaged cells — such as cell senescence and regulated cell death — are all coupled with the generation of signals that elicit microenvironmental and/or systemic responses. Such mechanisms of cellular adaptation to stress contribute to the formidable resilience of the organism but can also contribute to its degeneration over time. 3

Normally in cells there exists equilibrium between pro-oxidant species and antioxidant defense mechanisms such as ROS-metabolizing enzymes including catalase, glutathione peroxidase, and superoxide dismutases (SODs) and other antioxidant proteins such as glutathione (GSH)

For the preservation of organismal homeostasis, as severely damaged, irreversibly infected, functionless and/or potentially oncogenic cells are destined for persistent inactivation or elimination, respectively.

It has become apparent that most (if not all) mechanisms of cellular response to stress are also associated with paracrine and endocrine signals that communicate a potential threat to the organism and hence contribute to the maintenance of systemic homeostasis. 

Why Darwin was wrong, and what really drives small adaptations ( microevolution ), and descent with modification Eo1NBW7
Signaling pathways and regulators of PRRs. 
Pattern-recognition receptors (PRRs) share intracellular pathways that lead to the production of pro-inflammatory cytokines and type I interferons (IFNs). 
a | All the Toll-like receptors (TLRs), except for TLR3, interact with MYD88 to induce the activation of nuclear factor-κB (NF‑κB) and mitogen-activated protein kinases (MAPKs), which induce the transcription factor activator protein 1 (AP-1), for the induction of pro-inflammatory cytokine expression. The TIR domain-containing adaptor protein inducing IFNβ (TRIF) pathway is shared by TLR4 and TLR3, and induces the activation of interferon regulatory factors IRF3–IRF7 for the production of type I IFNs.
b | Retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated protein 5 (MDA5) first interact with mitochondrial antiviral signaling protein (MAVS) and then activate signaling cascades through stimulator of interferon genes (STING) and TANK-binding kinase 1 (TBK1), leading to the expression of type I IFNs. MAVS also signals through receptor-interacting serine/threonine protein kinase 1 (RIPK1) for AP‑1 activation. 
c | Many cytosolic DNA and RNA sensors, including cyclic GMP–AMP synthase (cGAS), double-strand break repair protein MRE11, IFNγ-inducible protein 16 (IFI16), DNA-dependent protein kinase (DNA‑PK), the probable ATP-dependent RNA helicases DDX41 and DDX60, leucine-rich repeat flightless interacting protein 2 (LRRFIP2) and protein kinase RNA-activated (PKR), recognize intracellular DNA or RNA and converge on STING to drive type I IFNs and cytokine production. The ATP-dependent RNA helicases DHX9 and DHX36 recognize CpG-containing DNA and induce the MYD88‑dependent signalling pathway. 
d | NOD-like receptors (NLRs) are activated upon cellular infection or stress, and engage innate immune responses via RIPK2–NF‑κB signalling activation. Some NLRs, such as NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3), ICE protease-activating factor (IPAF) and NLR apoptosis inhibitory protein 5 (NAIP5), form inflammasomes that contain the apoptosis-associated speck-like protein containing a CARD (ASC) and caspase 1, and trigger the maturation of interleukin-1β (IL-1β). 4

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3081528/
2. https://www.hindawi.com/journals/ijcb/2010/214074/
3. http://sci-hub.tw/https://www.nature.com/articles/s41580-018-0068-0
4. http://sci-hub.tw/https://www.ncbi.nlm.nih.gov/pubmed/26711677


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