This powerpoint is made by Timothy G Standish and contains many interesting points of critique on the endosymbiotic theory. The link itself implies that this is for high school students, but I’ll recommend it to anyone interested in mitochondria. We should realize that things in biology only make sense in the light of evolution, and I think that this presentation (and my own site) add to the realization that we do ot yet know how mitochondria arose. The presentation contains many figures illustrating the problems.
He only discusses two hypotheses, one is the endosymbiotic theory and the second is the invagination of the plasma membrane. I think that there is a third possibility, explored on this web site in which mitochondria are specialized organelles, as a result from the gradual evolution ER>Golgi>vesicles driven by the separation and uncoupling of functions, in this case the partitioning of the potentially harmful energy generation.
The next point are often stated as evidence. I will also discuss these later on my site. I already started with the first point, namely that bacteria resemble mitochondria which is quite far from the truth as these pictures will show. I don’t know how any self-respecting biologist can repeat the claim that they resemble bacteria.
How Mitochondria Resemble Bacteria
Most general biology texts list ways in which mitochondria resemble bacteria. Campbell et al. (1999) list the following:
- Mitochondria resemble bacteria in size and morphology.
- They are bounded by a double membrane: the outer thought to be derived from the engulfing vesicle and the inner from bacterial plasma membrane.
- Some enzymes and inner membrane transport systems resemble prokaryotic plasma membrane systems.
- Mitochondrial division resembles bacterial binary fission
- They contain a small circular loop of genetic material (DNA). Bacterial DNA is also a circular loop.
- They produce a small number of proteins using their own ribosomes which look like bacterial ribosomes.
- Their ribosomeal RNA resembles eubacterial rRNA.
And how they don’t resemble bacteria. I think that there are many more examples.
How Mitochondria Don’t Resemble Bacteria
- Mitochondria are not always the size or morphology of bacteria
- Mitochondrial division and distribution of mitochondria to daughter cells is tightly controlled by even the simplest eukaryotic cells
- Circular mtDNA replication via D loops is different from replication of bacterial DNA (Lewin, 1997 p441).
mtDNA is much smaller than bacterial chromosomes.
- Mitochondrial DNA may be linear, examples include: Plasmodium, C. reinhardtii, Ochromonas, Tetrahymena, Jakoba (Gray et al., 1999).
- Mitochondrial genes may have introns which eubacterial genes typically lack (these introns are different from nuclear introns so they cannot have come from that source) (Lewin, 1997 p721, 888).
- The genetic code in many mitochondria is slightly different from bacteria (Lewin, 1997)
The next is of course the crux of it all. Lateral gene transfer must have been extensive, yet, there are no mechanisms for it in a gradual scenario of evolution.
Timing of Gene Transfer
- Because gene transfer occurred in eukaryotes lacking mitochondria, and these are the lowest branching eukaryotes known
- Gene transfer must have happened very early in the history of eukaryotes.
- The length of time for at least some gene transfer following acquisition of mitochondria is greatly shortened.
- No plausible mechanism for movement of genes from the mitochondira to the nucleus exists although intraspecies transfer of genes is sometimes invoked to explain the origin of other individual nuclear genes.
Lateral gene transfer is not so easy as it may seem. In my opinion, if it happened at all frequently, it needed to be orchestrated in order to get functional genes. I just don’t see how you could get a gene inserted at the right place, well-expressed and completely functional without affecting other genes at a random basis. Normally, genes inserted into a well-orchestrated developmental scheme would wreak havoc, causing more harm than good. This is apart from protein import as sketched here:
No Plausible Mechanism Exists
- If genes were to move from the mitochondria to the nucleus they would have to somehow pick up the leader sequences necessary to signal for transport before they could be functional
- While leader sequences seem to have meaningful portions on them, according to Lewin (1997, p251) sequence homology between different sequences is not evident, thus there could be no standard sequence that was tacked on as genes were moved from mitochondria to nucleus
- Alternatively, if genes for mitochondrial proteins existed in the nucleus prior to loss of genes in the mitochondria, the problem remains, where did the signal sequences come from? And where did the mechanism to move proteins with signal sequences on them come from?
The difference in codon assignment seems a real hurdle and I would say that it is impossible to get a mitochondrial gene into the nucleus without it loosing function due to codon assignments. Of course, a scenario in which there was no mito>nucleus gene transfer (as in eukaryotic origin hypothesis)
Variation In Codon Meaning
- Lack of variation in codon meanings across almost all phyla is taken as an indicator that initial assignment must have occurred early during evolution and all organisms must have descended from just one individual with the current codon assignments
- Exceptions to the universal code are known in a few single celled eukaryotes, mitochondria and at least one prokaryote
- Most exceptions are modifications of the stop codons UAA, UAG and UGA
- NOTE - This would mean AUA changed from Ile to Met, then changed back to Ile in the Echinoderms
- Changing the genetic code, even of the most simple genome is very difficult
- Because differences exist in the mitochondrial genomes of groups following changes in the mitochondrial genetic code, mitochondrial genes coding differently must have been transported to the nucleus.
- These mitochondrial genes must have been edited to remove any problems caused by differences in the respective genetic codes.
And he concludes that the endosymbiotic theory becomes improbable.
- Presence of mitochondrial genes in nuclear DNA reduces the window of time available for mitochondrial acquisition in eukaryotes.
- Understanding the structure of mitochondrial genes in the nucleus and how they are expressed makes the transfer of genes from protomitochondria to the nucleus appear complex.
- Differences between mitochondrial genetic codes and nuclear genetic codes adds to the complexity of gene transfer between mitochondria and nucleus.
- As molecular data accumulates, the endosymbiotic origin of mitochondria appears less probable.