The origin of mitochondria

Mitochondria

Endosymbiotic organelles, most notably mitochondria and chloroplasts, arguably represent the penultimate stage of cellular degradation. These organelles retain their own genomes, albeit with very few genes, their own internal translation systems and their own membranes, although substantially modified from the ancestral bacterial membranes.


The mitochondrion (plural mitochondria) is a membrane-bound organelle found in most eukaryotic cells (the cells that make up plants, animals, fungi, and many other forms of life). These structures are sometimes described as "cellular power plants" because they generate most of the cell's supply of adenosine triphosphate (ATP), used as a source of chemical energy. In addition to supplying cellular energy, mitochondria are involved in other tasks such as signaling, cellular differentiation, cell death, as well as the control of the cell cycle and cell growth.

Several characteristics make mitochondria unique. The number of mitochondria in a cell varies widely by organism and tissue type. Many cells have only a single mitochondrion, whereas others can contain several thousand mitochondria. The organelle is composed of compartments that carry out specialized functions. These compartments or regions include the outer membrane, the intermembrane space, the inner membrane, and the cristae and matrix. Mitochondrial proteins vary depending on the tissue and the species. In humans, 615 distinct types of proteins have been identified from cardiac mitochondria, whereas in rats, 940 proteins have been reported.The mitochondrial proteome is thought to be dynamically regulated. Although most of a cell's DNA is contained in the cell nucleus, the mitochondrion has its own independent genome. Further, its DNA shows substantial similarity to bacterial genomes.


http://www.evolutionnews.org/2012/01/on_the_origin_o054891.html


http://www.origin-of-mitochondria.net/?p=41

Bacterial cell membranes

http://www.origin-of-mitochondria.net/?p=205

Recent, Functionally Diverse Origin for Mitochondrial Genes from ~2700 Metazoan Species

http://www.answersingenesis.org/articles/arj/v6/n1/mitochondrial-genes

Abstract

On the Origin of Mitochondria: Reasons for Skepticism on the Endosymbiotic Story

http://reasonandscience.heavenforum.org/t1465-evidence-against-mitochondrial-endosymbiosis#2130

http://www.evolutionnews.org/2012/01/on_the_origin_o054891.html#sthash.7fllKWEP.dpuf

Such an evolutionary transition is far from trivial. Biologist Albert de Roos writes,

   In linear mitochondrial chromosomes various different mechanisms to "prevent" shortening exist, ranging from hairpin loops and self-priming to protein-assisted primer synthesis . The telomeric regions of mitochondrial chromosomes do not seem to have a direct phylogenetic relation since they use other proteins and mechanisms than nuclear telomeres. Thus, it is difficult to deduce evolutionary pathways purely based on phylogenetic data on telomeres and mechanisms for end replication.

The claim one often hears is that circular mitochondrial DNA replication resembles bacterial binary fission. While this is true, in at least some respects, there are also important differences. For example, many of the key components are of eukaryotic origin and replication beginning at the Displacement (D-) loop (Fish et al., 2004; Clayton, 1996) is not the same as bacterial DNA replication.

The Lack of a Mechanism

http://www.uncommondescent.com/intelligent-design/on-the-non-evidence-for-the-endosymbiotic-origin-of-the-mitochondria

By far the most potent challenge to the endosymbiotic origin of eukaryotic mitochondria is the lack of a viable mechanism, perhaps most particularly with respect to the transfer of genes from the mitochondrion to the nucleus.

All evolutionary theories must offer an explanation in mechanistic terms of how it should or could have happened in order to be tested. The difficult thing with the endosymbiotic theory is that it proposes no real mechanism and most textbooks show the simplistic picture of a cell that swallows another cell that becomes a mitochondrion. Unfortunately, it is not so simple as that. There is a difference between the process of endosymbiosis and its incorporation in the germline, necessitating genetic changes. What were those changes? What was the host? Was it a fusion, was it engulfment, how did the mitochondrion get its second membrane, how did two genomes in one cell integrate and coordinate? The theory is also strongly teleological, illustrated by the widely used term 'enslavement'. But how do you enslave another cell, how do you replace its proteins and genes without affecting existing functions? The existence of obligate bacterial endosymbionts in some present eukaryotes is often presented as a substitute for a mechanism, but they remain bacteria and give not rise to new organelles. So, before we can speak of the endosymbiotic as a testable scientific theory, we need a mechanistic scenario which is lacking at the moment.

When we do try to envision a mechanistic scenario based on the endosymbiotic theory, we quickly run into problems. Genetic mutations that allow bacteria to thrive in the cytoplasm would not be strategic for survival. Anaerobic cells normally do not survive in environment that contains oxygen, while the endosymbiont would need oxygen in order to present fitness advantage. The two organisms would initially compete for energy sources since bacteria are users of ATP and do not export it. The extensive gene transfer that is needed in the endosymbiotic theory would wreak havoc in a complex genome since frequent insertion of random pieces of mitochondrial DNA would disrupt existing functions. Furthermore, gene transfer is a multi-step process were genes need to be moved to the nucleus, the different genetic code of mitochondria needs to be circumvented, the genes need to be expressed correctly, as well as imported back into the mitochondria in order to be functional. All in all, mechanistic scenarios for the endosymbiotic theory imply many non-functional intermediates or would just be plain harmful to an organism.



It is frequently asserted that the double membrane of mitochondria provides evidence for its endosymbiotic origin. There are, however, important differences between bacterial and mitochondrial membranes. Albert de Roos observes,

   The bacterial membrane is one of the basic characteristics that distinguish bacteria from eukaryotes. In order for mitochondria to resemble bacterial membranes, they should share characteristics such as a cell wall with peptidoglycan and lipopolysaccharides, gram-staining and antibiotic sensitivity. Some effects of antibiotics have been seen with both bacteria and mitochondria, but the effect is minor while the use of antibiotics is based on the principle that they distinguish between bacteria and eukarytes, including the mitochondrion (here). Until then, the selection of a few apparent similarities while ignoring the many differences does not indicate a bacterial origin for mitochondria. On the contrary, the fact that their membranes are so different as well as the fact that nearly all genes are encoded by the nucleus is primarily evidence against a bacterial origin.

   Even though some shared characteristics may be found, we have to realize that bacterial and eukaryotic membranes are fundamentally different. It seems virtually impossible to change all fundamental bacterial membrane characteristics and replace them with a eukaryotic counterpart without loosing membrane integrity. The differences between the membranes of mitochondria and the cell walls of bacteria make the endosymbiotic theory mechanistically difficult. It seems quite clear that bacterial membranes do not change easily into other membranes, and frankly I don't see any scenarios in which to change all these membrane components without drastically affecting fitness.


The Size and Shape of Mitochondria

The argument based on the size and shape of mitochondria is one that has been turned on its head in recent years, being transformed from an argument for endosymbiosis to one against it. These organelles are now acknowledged in the literature to be better understood as dynamic reticular structures (see this link for references).

Electron micrographs displaying cross-sections of mitochondria portrayed the mitochondrion as a sphere. However, when one looks at 3D models of the organelle, the reality is somewhat different.

The Origin of Complex Life

Two greyscale transmission electron micrographs, which are labeled D and E, show mitochondria in different organisms. The photomicrograph in panel D shows a cross-section through a large dinoflagellate mitochondrion. Because the mitochondrion is folded, different parts of it look like stacked layers in the cross-section. The inner membrane is folded into hundreds of cristae, which look like inward-facing, finger-shaped projections. Panel E shows a cross-section of twelve mitochondria in a Paramecium cell. Each mitochondrion has either a circular or oval shape. The mitochondria are filled with inner membranes, which look like finger-shaped projections or small circles.

Despite their power, protons have their share of problems, and these problems might explain why life got stuck in a rut for 2 billion years. All complex life on Earth today is composed of a certain type of complex cell, known as a eukaryotic cell. Generally much larger than bacteria or archaea, the eukaryotic cell contains a nucleus, and a much larger genome, and all kinds of specialized organelles (little organs), such as mitochondria. The strange thing is that eukaryotes have repeatedly given rise to large, complex, multicellular organisms like plants, animals, fungi, and algae — but prokaryotes show little or no tendency to evolve greater morphological complexity, despite their biochemical virtuosity. Why not?
One possible answer relates to the control of proton gradients. All eukaryotic cells turn out to have mitochondria, or once had them and later lost them by reductive evolution back toward a prokaryotic state. No mitochondria, no eukaryotes (Figure 6). All mitochondria capable of oxidative phosphorylation have retained a tiny genome of their own, which appears to be necessary to maintain control over membrane potential (Allen 2003). A membrane potential of 150 mV across the 5-nanometer membrane gives a field strength of 30 million volts per meter — equivalent to a bolt of lightning. This huge electrochemical potential makes the mitochondrial membranes totally different from any other membrane system in the cell (such as the endoplasmic reticulum) which, according to Allen, is why mitochondrial genes are needed locally in cellular subregions. In effect, by responding to local changes in electrochemical potential, they prevent the cell from electrocuting itself. No mitochondrial genome, no oxidative phosphorylation. It could be, then, that bacteria can't expand in cell and genome size because they can't physically associate the right set of genes with their energetic membranes. Lacking mitochondria, bacteria cannot grow large and complex, because they can't control respiration over a wide area of energetic membranes (Lane & Martin, in press). If that's the case, the acquisition of mitochondria and the origin of complexity could be one and the same event.

The question is, what kind of a cell acquired mitochondria in the first place? Most large-scale genomic studies suggest that the answer is an archaeon — that is, a prokaryotic cell that is in most respects like a bacterium. That begs the question, how did mitochondria get inside an archaeon? The answer is a mystery but might go some way toward explaining why complex life derives from a single common ancestor, which arose just once in the 4 billion years of life on Earth.

https://www.nature.com/scitable/topicpage/why-are-cells-powered-by-proton-gradients-14373960/#:~:text=Recent%20research%20suggests%20that%20proton,as%20they%20do%20in%20cells.