How so? single-chromosome mutations can account for all variations one gets from the opposite sex, bad configurations can be selected against inside the germinal cells themselves or when the new organism is just a clump of a few thousand cells, which is how most “really bad” configurations get selected against in sexual organisms too.
bad configurations can be selected against inside the germinal cells themselves or when the new organism is just a clump of a few thousand cells
Many genes and downstream effects are only expressed (and can be selected on) after birthing/hatching, or only in adult organisms. This can include whole organs, e.g. mammal fetuses don’t use their lungs in the womb. A fetus could be deaf, blind, weak, slow, stupid—none of this would stop it from being carried to term. An individual could be terrible at hunting, socializing, mating, raising grandchildren—none of that would stop it from being born and raised to adulthood.
There’s no biological way to really test the effect of a gene ahead of time. So it’s very valuable to get genes that have already been selected for beneficial effects outside of early development.
That’s in addition to p.b.’s point about losing information.
Let’s say there is a section in a chromosome with 10 genes. In one chromosome 8 of these have damaging mutations. In the other chromosome these 8 are good copies but the other two are damaged. Now crossover of that section could fix the first chromosome by replacing 8 bad copies with 8 good copies and only 2 good copies with 2 bad copies. But going forward the resulting organism only has bad copies of these two genes.
In sexual reproduction there would be a large pool of correct copies out there and at some point these would be swapped back into this line. With cloning the information is lost for all descendants until random mutation recreates it.
Positive mutations would have to achieve for each germline what in sexual reproduction they have to achieve for just a few members of the entire species.
In sexual reproduction there would be a large pool of correct copies out there and at some point these would be swapped back into this line. With cloning the information is lost for all descendants until random mutation recreates it.
I think I get your point here, though I think this assumes a lot about how much cross-over mechanisms can actually “detect” genetic damage.
If this damage can mostly be detected only once the organism is mature enough to be selected for/against by “environment” then I think that kind of goes back into the “red queen” style theory that I’m a fan of (i.e. “hidden traits” that occasionally manifest in the population instead of dying out)
If this damage can mostly be detected at cross-over time or when the organism is still very young or in the germ cells themselves… then I’d expect this is also the kind of damage that won’t be present in germ cells to being with, or not in many because there’s already intra and inter cellular mechanisms to correct for this by inducing apoptosis in the damaged cell.
But maybe I’m missing something and I don’t understand the finer details of cross over well enough.
How so? single-chromosome mutations can account for all variations one gets from the opposite sex, bad configurations can be selected against inside the germinal cells themselves or when the new organism is just a clump of a few thousand cells, which is how most “really bad” configurations get selected against in sexual organisms too.
Many genes and downstream effects are only expressed (and can be selected on) after birthing/hatching, or only in adult organisms. This can include whole organs, e.g. mammal fetuses don’t use their lungs in the womb. A fetus could be deaf, blind, weak, slow, stupid—none of this would stop it from being carried to term. An individual could be terrible at hunting, socializing, mating, raising grandchildren—none of that would stop it from being born and raised to adulthood.
There’s no biological way to really test the effect of a gene ahead of time. So it’s very valuable to get genes that have already been selected for beneficial effects outside of early development.
That’s in addition to p.b.’s point about losing information.
Let’s say there is a section in a chromosome with 10 genes. In one chromosome 8 of these have damaging mutations. In the other chromosome these 8 are good copies but the other two are damaged. Now crossover of that section could fix the first chromosome by replacing 8 bad copies with 8 good copies and only 2 good copies with 2 bad copies. But going forward the resulting organism only has bad copies of these two genes.
In sexual reproduction there would be a large pool of correct copies out there and at some point these would be swapped back into this line. With cloning the information is lost for all descendants until random mutation recreates it.
Positive mutations would have to achieve for each germline what in sexual reproduction they have to achieve for just a few members of the entire species.
I think I get your point here, though I think this assumes a lot about how much cross-over mechanisms can actually “detect” genetic damage.
If this damage can mostly be detected only once the organism is mature enough to be selected for/against by “environment” then I think that kind of goes back into the “red queen” style theory that I’m a fan of (i.e. “hidden traits” that occasionally manifest in the population instead of dying out)
If this damage can mostly be detected at cross-over time or when the organism is still very young or in the germ cells themselves… then I’d expect this is also the kind of damage that won’t be present in germ cells to being with, or not in many because there’s already intra and inter cellular mechanisms to correct for this by inducing apoptosis in the damaged cell.
But maybe I’m missing something and I don’t understand the finer details of cross over well enough.