Filed under: Warning: contains molecules
Here’s something which follows on from this post about what happens when viruses infect photosynthetic bacteria in the oceans and also from this post about Craig Venter, I guess, in that he is one of the authors of the paper I’m talking about, and the fishing of vast numbers of DNA sequences out of the ocean on which this work depends is something that he has pioneered.
As I was saying in that previous post, viruses which attack photosynthetic bacteria don’t just carry “viral” genes — genes that code for the components of the virus. They code their own versions of “bacterial” genes — genes that the bacteria use in their everyday existence — too. Why bother? Obviously the bacteria already have their own copies of the bacterial genes, and by carrying these genes the viruses are making their genomes bigger and thus more costly to reproduce, which you would think was a bad thing. The answer must be that getting the bacteria to read the viral versions of the genes and thus produce the proteins they encode helps the virus reproduce.
Now a paper by Itai Sharon and a number of co-authors, mostly at the Technion in Israel, published in the new ISME Journal offers further evidence on the matter. They worked with DNA samples from the open ocean, and one of the things they were looking for was those which contained parts of the D1 protein, which is central to photosynthesis. They found a great many copies of versions of the D1 protein from viruses (which could be identified because they were flanked by viral, as opposed to bacterial, genes), and found that they differed systematically from the normally expressed native bacterial versions in two particular parts of the sequence.
The researchers interpret this in the same way that the authors of the Nature paper I blogged about before (people from Penny Chisholm’s lab at MIT, largely) do in a paper they published last year in PLoS Biology. That study showed that in some cases there is a marked preference among the viruses for forms of the D1 protein that look like the forms which some of their hosts keep in reserve for times of stress. It looks quite likely that these viral proteins undergo less turnover than the normal proteins. I imagine they probably pay for this in terms of increased damage and lower efficiency in the long run, but make up for that by requiring less maintenance effort. That’s a good short-term trade-off for a cell with other stresses to deal with — and its a neat trick to steal if you’re a virus that wants to devote as much of your host cell’s capabilities as possible to making more virus. The details of the differences between viral forms of the protein and the common bacterial forms seem to bear this analysis out.
This is not just a quirky thing. Bacterial photosynthesis counts for a significant part of total ocean productivity, and a few percent of those bacteria will, at any given time, be under viral control, and probably expressing viral photosynthesis proteins. The idea that a measurable chunk of the earth’s primary productivity is in the hands of the viruses strikes me as quite a cool one.
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