When you get an allele from sex, there are two sources of variance. One is genes your (adult) partner has that are different from yours. The other is additional de novo mutations in your partner’s gametes.
The former has already undergone strong selection, because it was part of one (and usually many) generations’ worth of successfully reproducing organisms. This is much better than getting variance from random mutations, which are more often bad than good, and can be outright fatal.
Selecting through many generations of gametes, like (human) sperm do, isn’t good enough; it doesn’t filter out bad mutations in genes that aren’t expressed in sperm cells.
Lateral gene transfer might be as good as sex, but I don’t see how higher mutation rates can compete. I believe that empirically, mutations that weaken one of the anti-mutation DNA preservation mechanisms in gametes are usually deleterious and are not selected.
One is genes your (adult) partner has that are different from yours. The other is additional de novo mutations in your partner’s gametes.
Neither of which are guaranteed to yield viable offspring, the latter won’t carry all or maybe any of the benefits when mixed with your genes. Indeed, chances are most won’t.
On the other hand just getting random mutation on a constant set of genes seems like it has a much higher chance of still yielding a viable combination.
The former has already undergone strong selection, because it was part of one (and usually many) generations’ worth of successfully reproducing organisms
How many generations of reproduction do you get in-absentia of recombination with other lineages between they are no longer compatible sexually? The answer varies based on the mutation rate, but it boils down to “surprisingly few”.
A lineage getting a new mutation often results in speciation.
Also, see, most mammals mate with individuals on average 1 to 10 generations removed from them with few exceptions in rather “primitive” animals.
Selecting through many generations of gametes, like (human) sperm do, isn’t good enough; it doesn’t filter out bad mutations in genes that aren’t expressed in sperm cells.
Why? The vast majority of potential children in most mammals die because of structural issues that are “detected” very early on (i.e. at the stage when they are still a clump of cells). One reason why old animals become infertile even if germinal cells are still present.
Could this mechanism not do any better?
More importantly, I think you’re missing the point when I say “in some species the vast majority of resources go towards mate selection”. Get rid of that and allow every individual to reproduce and you’d get the ability to have many more offsprings to “test” stuff in.
Lateral gene transfer might be as good as sex, but I don’t see how higher mutation rates can compete. I believe that empirically, mutations that weaken one of the anti-mutation DNA preservation mechanisms in gametes are usually deleterious and are not selected.
Some bacteria and archaea do little to not LGT, many viruses don’t either. They have been here for potentially billions of years and will likely outlive.
The same can be said for many plants that reproduce mainly via cloning.
If you want to take a homo-centric POV and assume we are the end-all-be-all of biological life, fine, but even then you ought to keep in mind that sex might not be a requirement for that. Other strategies exist, and they don’t involve sexual reproduction, the fact they did not evolve us may be chance
At any rate, I think your view might be mostly right, but it’s not the view I was arguing against. But I think you’re still missing the point if you have any reasonable certainty this explains sex in a satisfactory (see my reply for why). But you can be mostly right and still miss most things that are interesting, critical, give predictive power and best describe a phenomenon.
Sex is necessary to avoid Müller’s ratchet if you can’t have a gazillion offspring. Müller’s ratchet is not avoided by introducing more variance (at least that’s a very weird way to look at it). It is avoided by getting “undamaged” genes for your “damaged” ones and “fixing” your chromosome by recombination. (Of course this only happens randomly, but then there’s selection on top.)
The strategy of trying many mutations in many offspring just doesn’t work for very complex organisms. And higher mutation rates just speed up Müller’s ratchet.
Without sex and recombination you’d need an insane amount of selection to counteract mutation.
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.
When you get an allele from sex, there are two sources of variance. One is genes your (adult) partner has that are different from yours. The other is additional de novo mutations in your partner’s gametes.
The former has already undergone strong selection, because it was part of one (and usually many) generations’ worth of successfully reproducing organisms. This is much better than getting variance from random mutations, which are more often bad than good, and can be outright fatal.
Selecting through many generations of gametes, like (human) sperm do, isn’t good enough; it doesn’t filter out bad mutations in genes that aren’t expressed in sperm cells.
Lateral gene transfer might be as good as sex, but I don’t see how higher mutation rates can compete. I believe that empirically, mutations that weaken one of the anti-mutation DNA preservation mechanisms in gametes are usually deleterious and are not selected.
Neither of which are guaranteed to yield viable offspring, the latter won’t carry all or maybe any of the benefits when mixed with your genes. Indeed, chances are most won’t.
On the other hand just getting random mutation on a constant set of genes seems like it has a much higher chance of still yielding a viable combination.
How many generations of reproduction do you get in-absentia of recombination with other lineages between they are no longer compatible sexually? The answer varies based on the mutation rate, but it boils down to “surprisingly few”.
A lineage getting a new mutation often results in speciation.
Also, see, most mammals mate with individuals on average 1 to 10 generations removed from them with few exceptions in rather “primitive” animals.
Why? The vast majority of potential children in most mammals die because of structural issues that are “detected” very early on (i.e. at the stage when they are still a clump of cells). One reason why old animals become infertile even if germinal cells are still present.
Could this mechanism not do any better?
More importantly, I think you’re missing the point when I say “in some species the vast majority of resources go towards mate selection”. Get rid of that and allow every individual to reproduce and you’d get the ability to have many more offsprings to “test” stuff in.
Some bacteria and archaea do little to not LGT, many viruses don’t either. They have been here for potentially billions of years and will likely outlive.
The same can be said for many plants that reproduce mainly via cloning.
If you want to take a homo-centric POV and assume we are the end-all-be-all of biological life, fine, but even then you ought to keep in mind that sex might not be a requirement for that. Other strategies exist, and they don’t involve sexual reproduction, the fact they did not evolve us may be chance
At any rate, I think your view might be mostly right, but it’s not the view I was arguing against. But I think you’re still missing the point if you have any reasonable certainty this explains sex in a satisfactory (see my reply for why). But you can be mostly right and still miss most things that are interesting, critical, give predictive power and best describe a phenomenon.
I think Dan is correct.
Sex is necessary to avoid Müller’s ratchet if you can’t have a gazillion offspring. Müller’s ratchet is not avoided by introducing more variance (at least that’s a very weird way to look at it). It is avoided by getting “undamaged” genes for your “damaged” ones and “fixing” your chromosome by recombination. (Of course this only happens randomly, but then there’s selection on top.)
The strategy of trying many mutations in many offspring just doesn’t work for very complex organisms. And higher mutation rates just speed up Müller’s ratchet.
Without sex and recombination you’d need an insane amount of selection to counteract mutation.
having pairs of chromosomes and crossover are sufficient to resolve it
Do you mean cloning instead of sexual reproduction but with two chromosomes and crossover? That wouldn’t be enough to avoid mutational meltdown.
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.