On The Non-Evidence For The Endosymbiotic Origin Of The Mitochondria
|March 9, 2011||Posted by Jonathan M under Intelligent Design|
Over the past several weeks, I have been reviewing the case presented by Daniel Fairbanks for common ancestry in his 2010 book, Relics of Eden. For my previous articles on this topic, see my discussion of the first three chapters here, here and here. Chapter 4 of Fairbanks’ book is entitled “Solving The Trichotomy”. In this chapter, Fairbanks addresses what he calls the “trichotomy problem”— that is, of humans, chimpanzees, and gorillas, which two of the three are most closely related to each other? In the latter half of his chapter, Fairbanks draws evidence from mitochondrial DNA and nuclear DNA studies in support of the traditional view that humans and chimpanzees are the closest genetically related. Before turning to this question, however, Fairbanks offers an array of evidence in view of confirming the standard evolutionary view that the mitochondrion is derivative of alpha-proteobacteria and became incorporated into the now-eukaryotic cell by virtue of an endosymbiotic event. I am going to divide my discussion of this chapter into two separate articles — in the first (this article), I am going to address the purported case for the endosymbiotic origin of mitochondria. In the second, I will discuss Fairbanks’ comments on the “trichotomy problem”.
When I held my former views on common ancestry, I was greatly compelled by the array of evidence often marshalled in support of the endosymbiotic origin of the eukaryotic mitochondrion. Indeed, if such a claim is true, then the proposition of the common ancestry of all eukaryotic life seems to be close at hand. This, I think, is an important area to discuss, for the argument — if sound — does not only establish the common ancestry of our order, primates. It also serves to support the somewhat grander claim that all extant eukaryotes are derivative of a common ancestral progenitor. But the important and fundamental question must be raised: Is this argument sound? Does the evidence support this claim? It is to this question that I now turn.
Does The Evidence Support The Endosymbiotic Hypothesis?
Fairbanks, in my opinion, does not marshall the strongest possible case in support of this popular hypothesis, instead largely appealing to DNA evidence which seemingly indicates that the Rickettsiae is the closest living relative of the mitochondria. He also tells us,
Modern bacteria species within this group live, grow, and divide naturally within eukaryotic cells, much like mitochondria do. Unlike mitochondria, they can briefly escape from their host cells and infect other cells. They often live within the cells of ticks, mites, chiggers, and fleas. Bites from these pests can transmit Rickettsiae and cause diseases such as Rocky Mountain spotted fever and epidemic typhus.
As I noted here, there is some seemingly confirmatory evidence which, at first brush, appears to corroborate this claim. For example, many eukaryotic mitochondria contain a single circular genome, carry out transcription and translation within its compartment, use bacteria-like enzymes/components, and replicate independently of host cell division and in a manner akin to bacterial binary fission. As with all the other apparent evidences for common ancestry, however, upon closer inspection, the evidence very quickly evaporates.
The Lamarckian Underpinnings Of Endosymbiosis
The first striking thing about this popular claim is its marked Lamarckian underpinnings, an old idea which maintains the concept of the inheritance of acquired characteristics (a view which is now at odds with a modern understanding of genetics). As I noted in the article linked above, unless there is a genetic basis for ensuring the propagation of the incorporated mitochondrial cell, there is no reason to think that it will be passed on in any hereditary fashion. Indeed, most of the mitochondrial genome has now been transitioned to the nucleus. But here’s the thing: the mitochondrial DNA has an extremely limited time to integrate with the DNA of the host cell. Otherwise, there is no reason to think that such an organelle could be passed on to proceeding generations, much less assimilated to undertake many critical energy-generating tasks of eukaryotic cells.
I also noted in the article linked above that a second problem with this scenario is that mitochondria use a slight variation on the conventional genetic code (for example, the codon UGA is a stop codon in the conventional code, but encodes for Tryptophan in mitochondria). This implicates that the genes of the ingested prokaryotes would need to have been recoded during the course of their transfer to the host cell’s DNA. Bear in mind that this is no simple process. Besides the re-coding of the mitochondrion (so as to comply with the conventional code), the genes would be required to be expressed correctly, as well as imported back into the mitochondrion in order to have any function. The situation becomes even worse when one considers that, in eukaryotic cells, a mitochondrial protein is coded with an extra length of polypeptide which acts as a “tag” to ensure that the relevant protein is recognised as being mitochondrial and dispatched accordingly. Moreover, the transfer of mitochondrial DNA to the host cell’s DNA would need to occur without any detriment to the host cell, in order to yield even a viable organism, let alone confer selective utility. The significant number of specific co-ordinated modifications which would be required to facilitate such a transition, therefore, arguably make it exhibitive of irreducible complexity.
I also cited a review paper which appeared in Nature a few months ago by the scientists Nick Lane and Bill Martin, which effectively demonstrated that the prokaryote-to-eukaryote transition was effectively impossible without the energy demands, pertinent to the biggest event of gene manufacture (second only to the origin of life) in the history of life on earth, being met by the mitochondrial processes of oxidative phosphorylation and the electron transport chain. These energy demands cannot be met by the bacterial cell alone.
The Cherry Picked “Evidence” For Endosymbiosis
As noted, one of the core arguments for endosymbiosis is its circular genome. What is often not noted, however, are the cases where eukaryotic mitochondria have linear genomes with eukaryotic telomeres. For example, one paper published in Trends in Genetics in 1998 noted that,
At variance with the earlier belief that mitochondrial genomes are represented by circular DNA molecules, a large number of organisms have been found to carry linear mitochondrial DNA. Studies of linear mitochondrial genomes might provide a novel view on the evolutionary history of organelle genomes and contribute to delineating mechanisms of maintenance and functioning of telomeres. Because linear mitochondrial DNA is present in a number of human pathogens, its replication mechanisms might become a target for drugs that would not interfere with replication of human circular mitochondrial DNA.
For further reading, see also this paper.
Another common argument for the endosymbiotic origin of the mitochondrion is its division by mechanisms akin to binary fission. What is often not noted, however, is that the mechanisms by which mitochondria replicate is not the same as those utilised by bacteria — indeed, it’s really quite different. In fact, many components of uniquely eukaryotic origin are used in this process. For a discussion of mitochondrial replication of a linear genome, see this PNAS paper.
Does Genetic Evidence Support Endosymbiosis?
As Fairbanks notes, genetic studies might reveal the presence of gene homologues in bacterial species. But here we are back to the “similarity = common ancestry” line of argumentation. It is only to be expected that biological systems, designed to carry out similar functions, will possess similar genetic makeup. Moreover, particularly when discussing bacterial phylogenies based on homologous genes, caution is warranted. Processes of lateral gene transfer readily upset classic tree topologies, and bacterial phylogenies are notoriously inconsistent (for why, see here and here).
To conclude, while one can find examples of similarity between eukaryotic mitochondria and bacterial cells, other cases also reveal stark differences. In addition, the sheer lack of a mechanistic basis for mitochondrial endosymbiotic assimilation ought to — at the very least — cause us to raise an eyebrow and expect some fairly spectacular evidence for the claim being made. At present, however, such evidence does not exist — and justifiably gives one pause for scepticism.