[Update: Waking up this morning I find that the ICR article this was based on has vanished (it may still return at a later date). I have a zotero capture if anyone wants a full copy of it.] [Update #2: It is indeed back now, and I’ve added a TL;DR summary at the bottom.]
In mammals (including humans) most DNA gets mixed together as it gets passed on from generation to generation: chromosomes come in pairs, one from the mother and the other from the father; but when sperm and eggs are produced these chromosomes swap segments, and the chromosome that ends up in a given sperm or egg is entirely random. There are two exceptions to this rule. Mitochondrial DNA (mtDNA) can only be inherited from the mother – though both sexes have it – while the “Y chromosome” is only passed down from father to son.
This property makes these two varieties of DNA extremely useful in tracing ancestry, as distinct lineages can be found and compared. When these lineages are traced backwards they can only merge, never split, and thus will eventually converge to a point. The human mitochondrial genome has famously been traced back to “Mitochondrial Eve,” who lived between somewhere 140 and 240 thousand years ago, probably in Africa. “Y-chromosomal Adam” (which doesn’t roll off the tongue quite as well) meanwhile is only dated to around 60 to 140 thousand years before the present, but lived on the same continent. Continue reading →
Now it’s my turn to be smug. In last month’s edition of Acts & Facts “Deputy Director for Life Sciences Research” Nathaniel Jeanson announced that he was investigating differential mutation rates as an explanation for the observed differences in sequence in the same gene in different species. His hypothesis was that God had, in effect, a pool of genes to choose from when he created life. All organisms that needed a specific gene would be given the same one, but the particular genes needed by each would vary. These originally identical genes would then diverge through mutations, with Jeanson using lower generation times as proxies for higher mutation rates. His original supporting evidence came in the form of the mitochondrial ATP-6 genes of the elephant, mouse, and fruit fly.
As I pointed out at the time there are a number of flaws in this hypothesis. For one – despite Jeanson’s claims to the contrary – this process would not necessarily create the observed hierarchy in sequence similarity. More importantly, however, the three animals analysed at that point just happened to have their evolutionary relatedness approximately agree with the predictions of Jeanson’s differential mutation rate model. I predicted that the mere insertion of a fourth animal would ruin the correlation, suggesting a turtle as a good test subject.
That is to say, according to some studies that a recent paper in Nature cites, an enzyme used in mitochondrial DNA transcription is “distantly related” to that of Bacteriophage T7 (a virus which infects E. coli), a similar enzyme that does the same thing in chloroplasts, and Pol I polymerases generally (whatever they are). This paper itself adds to the table the 3D structure of the human version of the enzyme.