I’m not sure from your essay what you mean by group selection at all.
Group selection, as I’ve heard it explained before, is the idea that genes spread because their effects are for the good of the group, or species. The whole point of evolution is that genes do well because of what they do for the survival of the gene. The effect isn’t on the group, or on the individual, the species, or any other unit other than the unit that gets copied and inherited.
The question that seems obvious is how self-incompatibility ever evolved in the first place, It must have arisen in a species that was self-compatible, and then gradually have risen to fixation in that species. The opposite can happen.
Let’s look at this from the point of view of a gene. Suppose a particular mutation in a single gene results in self-compatibility. What’s the story for the gene? Let’s suppose that it gives an overwhelming advantage over outside genes in fertilising itself, plus a normal chance at fertilising others. That gene ought to do well.
Well, maybe. If the plant has a typical set of recessive genes in its genome, self-fertilisation is a disaster. A few generations down the line, the self-fertilising plant will have plenty of genetic problems arising from recessive gene problems, and will probably die out. This means that self-fertilisation is bad—a gene for self-fertilisation will only prosper in those cases where it’s not fertilising itself.
So let’s change the scenario and assume the self-fertiliser manages to create a clone instead. Now many plants actually do cloning—it’s not inherently a bad idea. But even a good clone is not as good as a gene pool. Your neighbouring plants further up the hill might have specific adaptations to the soil up there that yours doesn’t have. The self-cloning plant can’t live there. Further south, where the climate is different—your clone won’t grow there. It will not spread throughout a whole range of environments as well as a species with an established gene pool can.
The general theme of clones is that they do very well for a while. But they can’t spread outside their original environment because they can’t reshuffle genes from the general gene pool. Then some disease springs up. Either it kills none of the clones, or essentially all of them. The regular gene pool suffers some losses, but has some survivors too.
Flowering is optional, but survival is compulsory. When times are hard, you put off sexual reproduction until later, and do just as well as any clone ever could. In really tough times, the variations in the sexual plants may prove to be the difference (for some of them) between survival and death, whilst all the clones end up perishing.
So many plants do a bit of both. They clone themselves when the going is good. Then they reproduce sexually after a while, when the benefits of rearrangement outweigh the costs of all the pollen, flowers etc. There are benefits, otherwise they wouldn’t bother.
Group selection, as I’ve heard it explained before, is the idea that genes spread because their effects are for the good of the species. The whole point of evolution is that genes do well because of what they do for the survival of the gene. The effect isn’t on the group, or on the individual, the species, or any other unit other than the unit that gets copied and inherited.
Group selection is group selection: selection of groups. That means the phenotype is group behavior, and the effect of selection is spread equally among members of the group. If the effect is death, this eliminates an entire group at once—and the nearer a selfish gene approaches fixation, the more likely it is to trigger a group extinction. Consider what would happen if you ran Axelrod’s experiments with group selection implemented, so that groups went extinct if total payoff in the group below some threshold.
The key point is nonlinearity. If the group fitness function is a nonlinear function of the prevalence of a gene, then it dramatically changes fixation and extinction rates.
Well, maybe. If the plant has a typical set of recessive genes in its genome, self-fertilisation is a disaster. A few generations down the line, the self-fertilising plant will have plenty of genetic problems arising from recessive gene problems, and will probably die out. This means that self-fertilisation is bad—a gene for self-fertilisation will only prosper in those cases where it’s not fertilising itself. It will do worse.
No. Self-fertilisation doesn’t prevent cross-fertilisation. The self-fertilizer has just as many offspring from cross-fertilization as the self-sterile plant, but it has in addition clones of itself. Many of these clones may die, but if just one of them survives, it’s still a gain.
I’m not sure from your essay what you mean by group selection at all.
Group selection, as I’ve heard it explained before, is the idea that genes spread because their effects are for the good of the group, or species. The whole point of evolution is that genes do well because of what they do for the survival of the gene. The effect isn’t on the group, or on the individual, the species, or any other unit other than the unit that gets copied and inherited.
The question that seems obvious is how self-incompatibility ever evolved in the first place, It must have arisen in a species that was self-compatible, and then gradually have risen to fixation in that species. The opposite can happen.
Let’s look at this from the point of view of a gene. Suppose a particular mutation in a single gene results in self-compatibility. What’s the story for the gene? Let’s suppose that it gives an overwhelming advantage over outside genes in fertilising itself, plus a normal chance at fertilising others. That gene ought to do well.
Well, maybe. If the plant has a typical set of recessive genes in its genome, self-fertilisation is a disaster. A few generations down the line, the self-fertilising plant will have plenty of genetic problems arising from recessive gene problems, and will probably die out. This means that self-fertilisation is bad—a gene for self-fertilisation will only prosper in those cases where it’s not fertilising itself.
So let’s change the scenario and assume the self-fertiliser manages to create a clone instead. Now many plants actually do cloning—it’s not inherently a bad idea. But even a good clone is not as good as a gene pool. Your neighbouring plants further up the hill might have specific adaptations to the soil up there that yours doesn’t have. The self-cloning plant can’t live there. Further south, where the climate is different—your clone won’t grow there. It will not spread throughout a whole range of environments as well as a species with an established gene pool can.
The general theme of clones is that they do very well for a while. But they can’t spread outside their original environment because they can’t reshuffle genes from the general gene pool. Then some disease springs up. Either it kills none of the clones, or essentially all of them. The regular gene pool suffers some losses, but has some survivors too.
Flowering is optional, but survival is compulsory. When times are hard, you put off sexual reproduction until later, and do just as well as any clone ever could. In really tough times, the variations in the sexual plants may prove to be the difference (for some of them) between survival and death, whilst all the clones end up perishing.
So many plants do a bit of both. They clone themselves when the going is good. Then they reproduce sexually after a while, when the benefits of rearrangement outweigh the costs of all the pollen, flowers etc. There are benefits, otherwise they wouldn’t bother.
Group selection is group selection: selection of groups. That means the phenotype is group behavior, and the effect of selection is spread equally among members of the group. If the effect is death, this eliminates an entire group at once—and the nearer a selfish gene approaches fixation, the more likely it is to trigger a group extinction. Consider what would happen if you ran Axelrod’s experiments with group selection implemented, so that groups went extinct if total payoff in the group below some threshold.
The key point is nonlinearity. If the group fitness function is a nonlinear function of the prevalence of a gene, then it dramatically changes fixation and extinction rates.
No. Self-fertilisation doesn’t prevent cross-fertilisation. The self-fertilizer has just as many offspring from cross-fertilization as the self-sterile plant, but it has in addition clones of itself. Many of these clones may die, but if just one of them survives, it’s still a gain.
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