Eliezer, I have to admit I’m not studied on the field enough, and I’ve not read papers on this particular. The initial cell bodies of a gamete of course come from the parent cell.
However after that, they have to keep on living. And they do this using their own genetic material to support and repair themselves, manufacturing new cell bodies, enzymes and other constituting proteins as old bodies deterioriate. All ovum in ovaries are present at birth of the female, thus having to be able to maintain their function at least up to menopause. This makes them one of the longest living cells beside neurons, while being haploid at that. Of course, as far as protein synthesis goes, I dont think this feat requires the usage of that great percentage of all genes after all, but it’s something anyway.
On the other hand, in the germ line there is a development phase from a fertilized ovum to the new gonads, where the germ line DNA is carried across multiple divisions in singular line. This accumulates more of said mutations, while selecting only against the most destructive mutations which express themselves in a relatively short period of time (the germ line cells are stem cells up to when gonad cells start to actually differentiate, and the differentiation obviously begins from more or less healthy stem cells at that point). Still, on the whole, this increases the corruptive pressure.
However, what I find more interesting, is how the point mutations affect regulatory areas and relevant ‘junk’ DNA. But we just don’t know enough of the mechanics there.
This is my relevant contribution.
Other commenters have made interesting points on how small adverse effect mutations dont really spread out quickly in the population, and how when selection actually happens post birth, it often tends to be the result of a combined work of many such adverse mutations, not just one. In this case, one death removes, on the average, more than just one adverse mutation from the pool. I haven’t delved deeper into the subject so I can’t say if this contradicts the initial assumption of “one mutation, one death” or not, although to me it seems it does. Why wouldn’t it? My apologies if this is ignorant question, I would do the maths now myself, but it’s late and I need the sleep.
Eliezer, I have to admit I’m not studied on the field enough, and I’ve not read papers on this particular. The initial cell bodies of a gamete of course come from the parent cell.
However after that, they have to keep on living. And they do this using their own genetic material to support and repair themselves, manufacturing new cell bodies, enzymes and other constituting proteins as old bodies deterioriate. All ovum in ovaries are present at birth of the female, thus having to be able to maintain their function at least up to menopause. This makes them one of the longest living cells beside neurons, while being haploid at that. Of course, as far as protein synthesis goes, I dont think this feat requires the usage of that great percentage of all genes after all, but it’s something anyway.
On the other hand, in the germ line there is a development phase from a fertilized ovum to the new gonads, where the germ line DNA is carried across multiple divisions in singular line. This accumulates more of said mutations, while selecting only against the most destructive mutations which express themselves in a relatively short period of time (the germ line cells are stem cells up to when gonad cells start to actually differentiate, and the differentiation obviously begins from more or less healthy stem cells at that point). Still, on the whole, this increases the corruptive pressure.
However, what I find more interesting, is how the point mutations affect regulatory areas and relevant ‘junk’ DNA. But we just don’t know enough of the mechanics there.
This is my relevant contribution.
Other commenters have made interesting points on how small adverse effect mutations dont really spread out quickly in the population, and how when selection actually happens post birth, it often tends to be the result of a combined work of many such adverse mutations, not just one. In this case, one death removes, on the average, more than just one adverse mutation from the pool. I haven’t delved deeper into the subject so I can’t say if this contradicts the initial assumption of “one mutation, one death” or not, although to me it seems it does. Why wouldn’t it? My apologies if this is ignorant question, I would do the maths now myself, but it’s late and I need the sleep.