Filed under: Warning: contains molecules
There’s a fascinating paper in this week’s Nature (Lindell et al, Nature, 449, pp 83-86 (2007) doi:10.1038/nature06130) dissecting what must be one of the most frequent fatal biological interactions in the world: the infection of the photosynthetic bacterium Prochlorococcus Med4 by the virus, or “phage”, P-SSP7.
This sounds pretty obscure, but it is a commonplace thing. In fact it is unimagineably commonplace. Prochlorococcus is perhaps the most plentiful organism on the planet — the average millilitre of surface seawater contains about 100,000 of them. A quick and doubtless very dirty calculation suggests that there are more prochlorococcus in the earth’s oceans than there are atoms in your head (sources wiki, madsci, guesswork). In parts of the ocean that are nutrient poor (which is a lot of the ocean) these peculiarly small bacteria — sometimes called picoplankton — dominate primary photosynthetic production.
And while doing so they get a lot of viral infections — perhaps 2-3% of the entire population is torn apart by phages every day (that figure is actually from a paper about synechococcus, but I’m happy to go with orders of magnitude here). This all means that a virus infects one of these bacteria a trillion times every nanosecond. And this process, or rather something functionally very similar, has presumably been happening at a similar rate for billions of years.
As I said, unimagineably commonplace.
So what goes on? A team at MIT and other institutions (including Debbie Lindell, now at the Technion, Penny Chisholm, the scientist who first discovered prochlorococcus, and George Church, high-throughput sequencing guru) has looked into the problem by stopping the process of infection at various stages (by flash freezing the bacteria involved) and then looking to see what genes were being transcribed when.
The virus forces the bacterium to produce copies of itself; if it didn’t, it would be a very poor virus. And the way it gets to work is very familiar, in that it is very like the job that the phage T-7 does on lab favourite E. coli. The deep similarities between the strategies used in the gut (natural habitat of E coli) and the open ocean on bacteria that live in entirely different ways is, the authors point out, remarkable.
At the same time as it’s doing this, though, the virus is also transcribing a small set of genes which, though carried in the viral genome, describe proteins that are used by the bacterial metabolism. One of these proteins is D1, which is the protein at the heart of photosystem II, the molecular machine that strips electrons from water using sunlight and thus drives the whole photosynthetic process. The other proteins are also involved in photosynthesis and the cell’s ability to handle its energy. By making more of these proteins, the virus is giving the bacterial cell an energy boost — at exactly the time that it is also requiring the cell to make copies of teh viral genome, which uses a fair amount of energy.
Meanwhile, control of the genomes having been taken over by the virus (and there’s an ablative absolute unknown to Caesar) most of the bacterial genes are shut off to some extent, meaning the proteins the bacteria would normally be making to keep itself in business don’t get made. But though the activity of 1,716 genes gets turned down this way, the expression of 41 others actually goes up, some immediately after infection, some about two hours later.
Some of this is the bacteria’s attempt to do something about the infection. Some may be caused by the phage for its own purposes. Some of it may be things that were once adapatations against infection but which the virus has evolved to welcome, even to promote. The story is particularly involved with the hli gene family. These genes do something (not entirely clear to me what) to help photosynthesis along and allow the bacteria to deal with high light conditions. They get turned on when the phage first strikes — and then copies carried by the phage itself get turned on. What’s more, some of the versions of hli genes seen in bacterial genomes seem to have been acquired from phages and then put to bacterial use.
This is all fascinating (at least to me). And as the authors say, further work on these lines will probably have implications for understanding how bacterial photosynthesis works at an ecological level and what factors limit it. But it also seems to hint at something bigger or stranger. It is very hard for us to see this other than in terms of one thing attacking another. Its almost impossible to describe without terms of agency on the part of the players. But reading about it in this detail brings with it a sense in which teh infectuion almost feels like a thing in itself — a process to be described in its own terms, not as a struggle between two players. I suppose this feeling is linked to the ideas that drive “systems biology” — that there is a system here, phage+bacterium, that is its own thing, and can’t be reduced to two complex components, that evolves in its own way.
I’ve no idea whether that idea has much use or room for expansion; and it carries a vaguely Cronenbergy vibe I’m not necessarily on for. It just felt hard to avoid. The paper is fascinating regardless.
Image: Lawrence Berkeley Labs
1 Comment so far
Leave a comment