Mitochondria and plastids in eukaryotes evolved through a process of endosymbiosis. How does an event like a eukaryote engulfing a bacteria, become a part of the genome? Some of these primitive eukaryotes could have been more predisposed to more vigorous endocytosis as a result of their DNA, but how could the physical event account for evolution of organelles?

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    $\begingroup$ What exactly are you asking here? Mitochondria still have their own DNA, it's not in the "parent" cell. They reproduce on their own, it's just that they wait for the cell reproduction signals to do so. In fact, this is exploited in mapping female genealogies, since mitochondrial DNA is transferred predominantly through the female line (egg cells tend to carry a lot more mitochondria than sperm cells). $\endgroup$
    – Luaan
    Sep 21 '15 at 8:41

If your question is about how the engulfed endosymbionts lost their genes and became dependent on the host cell then this is the answer.

The current theory (Limited Transfer Window hypothesis) says that at some point, injury or membrane rupture of the endosymbionts would have resulted in the leakage of their genomic DNA. The host genome would have acquired these genes by a lateral gene transfer mechanism. Now, because the endosymbionts that have lost these genes randomly, would have a lower cost of maintenance (as they can acquire these gene products from the host cell) compared to those who still maintain these genes themselves, the former will outgrow the latter at some point. Note that there is a constraint on the population size and therefore there is a good chance that the endosymbionts with full set of genes, could go extinct because of their additional growth cost.

This is a probable way by which the endosymbionts lost their genes and became dependent on the host. It has been observed the number of genes transferred to the host correlates with the number of endosymbionts present in the cell. The rationale behind the limited transfer window hypothesis is that if the number of endosymbionts is high, then the likelihood for the host to tolerate damage to a few endosymbionts is higher (note that damage was the first step in the endosymbiont to host gene transfer).

This is still a hypothesis and the exact mechanisms are yet to be elucidated.


  1. Timmis, Jeremy N., et al. "Endosymbiotic gene transfer: organelle genomes forge eukaryotic chromosomes." Nature Reviews Genetics 5.2 (2004): 123-135.
  2. Smith, David Roy, Kate Crosby, and Robert W. Lee. "Correlation between nuclear plastid DNA abundance and plastid number supports the limited transfer window hypothesis." Genome biology and evolution 3 (2011): 365-371.
  3. Lane, Nick. "Plastids, genomes, and the probability of gene transfer." Genome biology and evolution 3 (2011): 372-374.
  4. Gray, Michael W. "Mitochondrial evolution." Cold Spring Harbor perspectives in biology 4.9 (2012): a011403.
  • $\begingroup$ Thanks for the information. I have a great deal more information than when I started. Rupture of the membrane could explain acquisition of the foreign DNA. $\endgroup$
    – user17496
    Sep 21 '15 at 9:38
  • $\begingroup$ @user17496 But you should bear in mind that it is just a hypothesis. This has not be explicitly proven. $\endgroup$
    Sep 21 '15 at 9:39
  • $\begingroup$ @WYSIWYG Once the DNA is out of the symbiont, it would likely be like transfecting a Eukaryotic cell today, easier as the symbiont is already in the cytoplasm. The chromosome would need to get into the nucleus. It would need to be linearized, and there would need to be an area of complementarity that would allow for strand invasion. The rest would be handled by the cells own repair mechanisms. Genes are maintained through selective pressure, and as you said, if it costs less to have the product produced by the host, then sustaining deleterious mutations will not be under selective pressure. $\endgroup$
    – AMR
    Sep 21 '15 at 13:11
  • $\begingroup$ @AMR Complementarity is not really essential. They can insert via a break and join mechanism. But as I said, we really do not know the mechanism yet. I don't think even the insertion hostpots have been studied in great detail. That reminds me; I should look for that. $\endgroup$
    Sep 21 '15 at 17:06
  • $\begingroup$ No, not essential, but I was thinking along the lines that there would be more opportunity for homologous incorporation than going down the path of NHEJ, especially to get a productive insertion where the gene is downstream of an active promoter, unless the entire gene "cassette" was inserted. Anyhow, my crystal ball gets very fuzzy after looking about a billion years back. 😉 $\endgroup$
    – AMR
    Sep 21 '15 at 17:23

I think you mean mitochondria and chloroplasts and are referring to the endosymbiont theory (Reference to the unedited question as it was originally asked).

The definition of symbiosis for the most part tells you how coevolution can be accounted for by this theory.

The larger Eukaryotes provided the protomitochondria with a protected environment for growth and the protomitochondria produced usable nutrients for their hosts from molecules that the eukaryotes were unable to process on their own.

The two organisms struck up a balance and the mutually beneficial relationship allowed both to prosper. As the Eukaryotes with protomitochondria were better able to utilize more of the chemicals from their environment than those that did not play host to the protomitochondria, they had a survival advantage that other early Eukaryotes did not.

As plant cells have both mitochondria and chloroplasts, it is believed that one of the eukaryotes with a mitochondria endocytosed a photosynthetic prokaryote. This event wasn't as much of an advantage as the first symbiotic relationship. Since all eukaryotes have mitochondria or evidence of ancestors that had mitochondria, but not all have chloroplasts, then it was beneficial enough that the photosynthetic organisms were also able to coevolve within the eukaryotes and alongside the mitochondria, but they were not beneficial enough so as to give those cells that hosted chloroplasts enough of an advantage that they took over all life on Earth.

Mitochondria also have their own DNA, so their complete genome is not found in the eukaryotic genome. Over evolutionary time, mitochondria have lost the genes that allowed them to live freely, so you could not extract them from eukaryotic cells today and expect them to grow external to the eukaryotic cell. They require substances that the eukaryotic cell makes. Whether there was recombination between the two genomes or just that both had the same function at one point and then through genetic drift caused the mitochondria to lose the homologous gene, I could not say.


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