Thursday, September 16, 2010

Bacterial mutability and a friendly apicomplexan

A few recent papers caught my attention. In the first, Chen et al. looked at an array of tandem repeats in DNA mismatch repair genes called MMR genes. These genes make proteins that allow bacteria (in this case Salmonella) to fix DNA mutations. Without functional MMR genes, bacterial populations become more variable because they can't repair their mutations. The weird thing is that tandem repeats can lead to mutations, which could inactivate the MMR genes. So the genes that repair DNA mutations are themselves liable to inactivation by mutation. What's the big deal? Well, we know that having a high mutability allows bacteria to adapt to new environmental conditions, and since MMR genes repair mutations, it makes sense that a population would want to shut off some MMR genes if they need to adapt. But you need the genes around generally, since a having a lot of mutations is harmful. Sure enough, Chen et al. found similar repeat sequences in the MMR genes of >100 bacterial genomes. Seems like this could be a common way for bacteria to switch between genetic stability (when MMR is working) and adaptability (when it isn't).

In the second paper, Saffo et al. report their discovery that the mutualistic Nephromyces is actually an apicomplexan. Nephromyces is found in the renal sacs of tunicates (or sea squirts) of the family Molgulidae, where it might be metabolizing urate. People have debated for some time what exactly Nephromyces is, but Saffo et al.'s results showing that it is an apicomplexan is somewhat surprising. There are about 5000 apicomplexan species described, and all of them except for Nephromyces are parasites. You're probably familiar with malaria, which is caused by the apicomplexan Plasmodium. In fact, Plasmodium is like the poster child for all the Apicomplexa in undergraduate textbooks. To a creationist like me, Nephromyces is interesting since it relates to the origin of disease and especially to the question of whether God created (or redesigned) organisms to cause disease at the Fall or whether previously helpful organisms merely became harmful over time.

Chen et al. 2010. Multiple genetic switches spontaneously modulating bacterial mutability. BMC Evolutionary Biology 10:277.

Saffo et al. 2010. Nephromyces, a beneficial apicomplexan symbiont in marine animals. PNAS

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