Wednesday 24 October 2012

Viruses have proteorhodopsin genes too!

Genomic techniques can reveal information on the evolution of proteorhodopsin

As Colin explained in our lecture this week, viral genomes can encode proteins which are not directly part of virus reproduction.  These extra proteins can modify functional systems of the infected cell to somehow aid, or boost, virus reproduction; a well-documented example of this being cyanophage which contain genes for photosynthesis. Viruses are thought to get these extra genes via horizontal gene transfer.

Yutin & Koonin (2012) have very recently found evidence that giant marine viruses have genes for proteorhodopsin, another light-dependant system with two different functions. The first being a light-driven proton pump which generates ATP, the second being a light-sensitive signal receptor potentially involved in phototaxis. It is useful to note at this point that it was only in the last decade that proteorhodopsins were discovered to be widespread in a diverse range of marine microbes and recognised as an important metabolic process in the oceans.

The authors analysed alignment of conserved sequence blocks in the rhodopsin super family (across viral, bacterial, archaeal and eukaryotic forms of the protein) and found that the viral sequence is highly conserved; however, it does not include the conservation of a proton donor. Therefore they conclude that without a proton donor, the function of the protein in the viral infected host is likely to be for sensory purposes, such as phototaxis, as opposed to being used as a light-driven proton pump. The alignment data then was used to construct a phylogenetic tree based on sequence similarity, authors were able to visualise distinct clades which infer that the giant virus acquired proteorhopsin from bacteria, or more likely eukaryotes, via horizontal gene transfer.

The authors quite rightly conclude that viral proteorhodopsins, regardless of their speculated function (signalling or proton pump), could be major players in virus-host ecology in the ocean. Looking at the bigger picture, maybe what these findings could potentially tell us about the evolution and conservation of proteorhodopsins is more interesting… It is clear that rhodopsins are an important protein as they are so highly conserved across different lineages, from the human eye, to bacterial proton pumps and now also found in viruses. Whilst it is likely that this protein evolved independently in both the eukaryotes and bacteria (and then diverged via horizontal gene transfer), more comparative and experimental work is needed in order to follow the evolution of this system; questions over its independent origins (or lack of) remain to be answered.

Yutin, N., & Koonin, E. V. (2012). Proteorhodopsin genes in giant viruses. Biology direct, 7(1), 34.

N.B. this paper has only just been accepted and is still "in press", only a provisional copy is available.


 

 

5 comments:

  1. Hi Vicky,
    I was wondering how the authors came to the conclusion that the virus acquired this gene from a bacterium or eukaryote and not the other way round?
    I've been reading a few (not particularly recent) papers that suggest that much of a giant virus's genome may be viral in origin (possibly predating eukaryotes), although there is not enough evidence to prove either theory.
    However it sounds like there may have been alot more interest in the gene the codes for proteorhodopsin and perhaps this is only a problem for some of the less studied genes...

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    1. Hi Hannah, thanks for your comment. It's hard to explain how they came to this conclusion as it was presented very visually, if go on the link and look at the phylogenetic tree it might help. Basically the positioning with in the phylogeny is often a good indicator of origin.
      I'm not sure I fully understand what you’re saying about acquiring it from a bacterium or eukaryote, or the other way round, are you saying that viruses existed before anything else? Please can you clarify.

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  2. wrong box- Great post Vicky.

    Two silly questions, I am a bit confused how the authors came to the conclusion that the role of proteodopsin in viral infected hosts is for sensory purposes? As you said in your post, There is a lack of conservation of the proton donor but why does this indicate sensory purposes? Would you mind clarifying that?

    Do you think the potenital roles of this protien could help us speculate viral "fitness" using genetic modification? Normally this method is shuned due to creating unnatural genetic variation but i think at this level, where horizontal gene transfer takes place, this method should be carried out.

    Thanks

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    1. Hi James, thanks for your comment they’re not silly questions at all, especially your question on fitness and genetic modification.
      The role of proteorhodopsins : sorry for the confusion there, I certainly could have made that bit clearer; perhaps I was being a little too concise. So, there are two main families of the proteorhodopsin protein, the first is a light driven proton pump like we discussed in the lecture with Colin, the second has a sensory function. Sensory rhodopsins have light sensitive receptors which provide the microbe with information about direction of light to produce a phototactic response. Because the genes in the giant virus don't encode a proton donor it is unlikely that the final product rhodopsin can function as a proton pump, the authors therefore conclude it’s the other type. The authors then proceed to come up with a nice story of how the viruses MIGHT use sensory rhodopsins for signalling purposes and particular phototaxis, which MIGHT trigger the movement of the host cell into areas rich in nutrients needed for viral reproduction.
      So now we're touching on your second question: could the function increase viral fitness? I deliberately steered away from this in my blog by saying "regardless of its function" as I don't think they have any evidence to back up their nice story about what the function MIGHT be. So no I don't think this study provides any evidence of fitness via genetic modification. However I think it would be good if an experiment could be designed, say to determine the function of viral proteorhodopsin and to test the hypothesis that proteorhodopsin genes increase viral fitness. Like you, I really do think that microbial life, particularly viruses, could be one of the most useful tools for evaluating and learning about evolution, unfortunately it seems that nobody in the current field is tackling these questions with the evolutionary rigour that we are being taught about by John.

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    2. Thank you for getting back to me and for clarifying my first question.

      As for the my second question i agree with you. I reviewed a paper 3 weeks ago which looked at the function of CtrA in the in magnetotactic bacteria. By Analysing its function compared to the function of CtrA in other alphaproteobacteria the authors construct a very nice hypothesis on how evolution might have occured in this huge phylum. If you have the time i would suggest reading it but i warn you it is heavy!

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