I have read quite some articles but I can't figure out the main reason for gc content deviation in prokaryotes. In eukaryotes I can understand it, because the genome isn't composed at random, like TATA boxes and CpG island, because they are important for functioning in the production of proteins.

However in prokaryotes there is such a variety, GC% is ranging from 20% up to 70%. Most of the time it depends on the environment, high temperature needs a stable genome (= high gc content).

I also read the answer to this question How does GC-content evolve? however it's still not clear to me. I hope someone can explain the deviation a little bit more.


Prokaryotes have an AT drift, but what mechanism causes some of these bacteria to higher their GC% instead of lowering it.

  • 2
    $\begingroup$ Possible duplicate of How does GC-content evolve? $\endgroup$
    – Forest
    Commented Apr 2, 2016 at 18:41
  • $\begingroup$ I have already read How does GC-content evolve, I even mentioned in mine question @Forest $\endgroup$
    – KingBoomie
    Commented Apr 3, 2016 at 11:02
  • $\begingroup$ Sorry, I should have seen that, @Rick Beelo! $\endgroup$
    – Forest
    Commented Apr 4, 2016 at 16:33
  • $\begingroup$ GC content is not related to optimal growth temperature. This theory has been refuted 15 years ago by many authors. The GC content of structural RNA (like 16S RNA) is indeed correlated to OGT, but not the GC content of the genome. See for example Galtier & Lobry (1997) ncbi.nlm.nih.gov/pubmed/9169555. $\endgroup$
    – user24495
    Commented Jun 15, 2016 at 11:08

2 Answers 2


I wonder whether it is just some sort of functionless drift. I don't know about bacteria, but think the example of some human viruses may be instructive. The human herpes simplex 1 virus (causes cold sores) has a very high GC content, whereas the quite closely related (in terms of gene repertoire and organization) human varicella zoster virus (causes shingles) has a bias towards AT. Now these viruses depend completely on the host cell's translational machinery, which will be similar (e.g. distribution of tRNA species) in the cells these two viruses infect (as will temperature, ionic strength etc.) (The viruses encode their own DNA replication enzymes but not the systems for transcription or translation.)

So if there is a functional reason for the differences in these alpha-herpes viruses, it is difficult to discern, and one might assume that the situation in bacteria might well be similar.

Clearly, there must be mechanisms for the accentuation in a GC bias once established. One imagines there could be a selective advantage in either replication, transcription or translation, but molecular explanations do not jump to mind (at least not to mine).

  • $\begingroup$ Interesting point about viral GC content, I never thought of that. As to bacteria, I could imagine a scenario, in which random drift affects DNA stability or replication/transcription efficiency, leading to a sub-population that's now better suited to some environment and in turn leading to speciation. Between genetic drift & selection pressure, though, we can paint a nice picture of evolution in general. =P $\endgroup$
    – Forest
    Commented Apr 2, 2016 at 18:40
  • $\begingroup$ There may be other factors involved with viruses of course. Perhaps what's important there is for the DNA to be different from the host for some reason. $\endgroup$
    – David
    Commented Apr 2, 2016 at 19:43
  • $\begingroup$ If we are talking about viruses, most of the time there is an bias towards A/T on the third position of the codon right? So the virus can adapt it's self to the tRNA pool of the host to speed up production of new virusses. @Forest $\endgroup$
    – KingBoomie
    Commented Apr 4, 2016 at 18:52
  • $\begingroup$ I don't know about the overall picture. Just those wretched herpesviruses which were such a pain to sequence. I think you need to be careful drawing conclusions as to why. Or at least recognize that a rationalization may seem plausible but have no experimental evidence to support it. And these herpesviruses show that tRNA availability need not be limiting. $\endgroup$
    – David
    Commented Apr 4, 2016 at 19:07
  • $\begingroup$ @RickBeeloo - I didn't know about the codon usage bias, so thanks for the TIL. Perhaps there's an evolved mechanism for codon usage bias in bacteria that affects GC content in different species. I found this paper (ncbi.nlm.nih.gov/pubmed/14659556) on the topic, which I won't have time to really read for a day or so. Might have some useful insights, though. $\endgroup$
    – Forest
    Commented Apr 4, 2016 at 19:09

Interesting question. I think that bacterial GC content diversity boils down to a mix of mutational biases, such as using different polymerase and replication/repair gene isoforms, and environmental pressures, such as temperature and salinity, that have placed different selection pressures on the various microbes.

I would read over the linked papers for more detailed info, but at least in broad strokes, I think that the two mechanisms listed above account for most of the observed variance.

NB: This isn't my main field, so you might get a more detailed answer if an actual microbiologist weighs in. :-)

  • $\begingroup$ You're welcome! Don't forget to vote up helpful answers. :-) $\endgroup$
    – Forest
    Commented Apr 4, 2016 at 16:32
  • $\begingroup$ Hahahha I'm new here :) @Forest $\endgroup$
    – KingBoomie
    Commented Apr 4, 2016 at 21:54

You must log in to answer this question.

Not the answer you're looking for? Browse other questions tagged .