Translation of mRNA into proteins is a nonstop, nonnegotiable process that is essential to the life of a cell, and it has acquired a *lot* of evolutionary tuning over the last few billion years. In critters like us with nuclei and other such organelles (the big happy club of eukaryotes, to which so many of my readers belong as G. K. Chesterton used to say), there’s a very important protein complex called elF4F.
That’s short for “eukaryotic initiation factor 4F", and it’s composed of three different subunit proteins. A lot of translation is “cap-dependent”, that is, it requires the presence of some special labels on the 5’ end of the messenger RNAs, and elF4F is what brings those capped RNAs together to the small (40S) ribosomal subunit to get things going. Prokaryotes, that is the bacteria, archaea, and of course the viruses that infect all the forms of life, don’t use elF4F or that mechanism. There are examples of viruses that express proteases that deliberately mess it up, the better to hijack the cell into making their own proteins instead, but that’s as close as you get.
Well, until now. This new paper comes from a team studying the (rather weird) “giant DNA viruses”. Those are odd beasts, not least because of their size. They can be visible by regular optical microscopy, and some of them are larger than some types of bacteria (!) They have large double-stranded DNA genomes, and these genomes code for some stuff that you just won’t find in any other viruses. There are enzymes in there that seem to come from glycolysis and tricarboxylic acid pathways, which is rather odd baggage for something that doesn’t actually have any metabolism of its own going on, and some of them also code for metabolic enzymes like CYP P450 subtypes. The belief is that some of these have been jacked from some ancient host cells at an earlier point in evolution and kept around ever since. Not least among their odd features is that these giant viruses can in turn be infected by virophages themselves: virus viruses! “Great fleas have lesser fleas, upon their backs to bite ‘em, and little fleas still lesser fleas, and so ad infinitum”.
We can add to that list of unnerving-for-a-virus features the presence of a viral form of elF4F! The authors here find giant DNA viruses deploying it as a weapon - it takes over for the host cell’s initiation factor complex but it only accepts viral RNA. So this allows the viral infection to roll along by co-opting the ribosomal machinery right from the very first stage. The paper shows that this vlF4F complex is also remarkably resistant to cellular stress, continuing to crank out viral proteins under all sorts of conditions.
This discovery (and the other odd genes mentioned above) really makes one think about what must be going on. It certainly does seem likely that such machinery was indeed stolen in the distant past from some eukaryotic cell that had already evolved them. But you certainly can’t rule out that infection by these giant DNA viruses, which are ubiquitous, have in turn affected eukaryotic evolution afterwards. Neither side is coming out of this unchanged, and untangling who has done what and to whom (and when!) is going to be quite the project. . .