-Mitochondrial DNA has 16,569 base pairs but only 13 of them code for protein (and most of those are dedicated to the electron transport chain, a pretty darn fundamental thing), so while the mutation rate of mtDNA is higher than nuclear DNA there’s a limited number of possible variations that will have an effect. There’s also a very constrained number of functional changes; most mutations of the protein-coding genes correspond to known mitochondrial diseases, which vary in their effects but do so on the basis of impaired mitochondrial activity globally. When mtDNA protein-coding regions shift, the result is usually one of the many known mitochondrial diseases, and it’s under those conditions that you see a strong variance in the expressed protein-coding mtDNA between different organs of the body. When mitochondrial genetics produces varying effects between different tissues, it’s not subtle—you’re basically talking about major, life-threatening illnesses or mosaic genetics here. Neither are common conditions; it’s difficult to imagine a functional shift in protein-coding for this producing a subtle effect that remains undetectable for a long time.
-mtDNA recombines with itself during reproduction, so mutations along the mitochondrial line are very easily tracked (indeed, it’s why we know what we do about human mitochondrial haplogroups, and why we can so readily understand which populations vary genetically by how much and when they seperated). Because one’s mtDNA is not specific to the individual, there’s a low effective population size for mtDNA changes While this does make it relatively easy for such changes to propagate upon mutation, it also makes them harder to miss when you go looking, and changes to protein-coding regions are even more obvious because there’s only a few of them and mutations to those usually affect very fundamental elements of cytochemistry.. The suggestion that IQ differences stem from a mitochondrial DNA shift implies that it would be very, very easy to spot and isolate the character responsible. We know a lot about mtDNA and the limited number of functional changes it displays. There’s nothing even vaguely like the proposed change sitting in the pool of known variations, and the pool of plausible unknown variations that just happen to look like that seems vanishingly small.
My prior is based on the following:
-Mitochondrial DNA has 16,569 base pairs but only 13 of them code for protein (and most of those are dedicated to the electron transport chain, a pretty darn fundamental thing), so while the mutation rate of mtDNA is higher than nuclear DNA there’s a limited number of possible variations that will have an effect. There’s also a very constrained number of functional changes; most mutations of the protein-coding genes correspond to known mitochondrial diseases, which vary in their effects but do so on the basis of impaired mitochondrial activity globally. When mtDNA protein-coding regions shift, the result is usually one of the many known mitochondrial diseases, and it’s under those conditions that you see a strong variance in the expressed protein-coding mtDNA between different organs of the body. When mitochondrial genetics produces varying effects between different tissues, it’s not subtle—you’re basically talking about major, life-threatening illnesses or mosaic genetics here. Neither are common conditions; it’s difficult to imagine a functional shift in protein-coding for this producing a subtle effect that remains undetectable for a long time.
-mtDNA recombines with itself during reproduction, so mutations along the mitochondrial line are very easily tracked (indeed, it’s why we know what we do about human mitochondrial haplogroups, and why we can so readily understand which populations vary genetically by how much and when they seperated). Because one’s mtDNA is not specific to the individual, there’s a low effective population size for mtDNA changes While this does make it relatively easy for such changes to propagate upon mutation, it also makes them harder to miss when you go looking, and changes to protein-coding regions are even more obvious because there’s only a few of them and mutations to those usually affect very fundamental elements of cytochemistry.. The suggestion that IQ differences stem from a mitochondrial DNA shift implies that it would be very, very easy to spot and isolate the character responsible. We know a lot about mtDNA and the limited number of functional changes it displays. There’s nothing even vaguely like the proposed change sitting in the pool of known variations, and the pool of plausible unknown variations that just happen to look like that seems vanishingly small.