There’s a lot to disentangle here, but I think you’re conflating embeddedness/constraint and I’m not sure what you are saying that invalidates my original point.
- re: embeddedness—the allele in a sexual species is shuffled into a wildly different background every generation whereas it the allele finds itself in a background which is almost the same every generation with the rare exception of horizontal gene transfer. A new mutation is very much embedded in a specific genetic background in a way that it is not in a sexual organism. For a mutation to be beneficial in a sexual organism, it needs to be beneficial on average across the vast pool of genomic combinations for that species—it can’t just be beneficial in the one genotype of the organism in which it occurred like it can in a clonal species. The mutation in a sexual organism also needs to be sexually beneficial in that particular gene pool, i.e. - a gene for red feathers is only good in a gene pool where the allele for attraction to red feathers is at a high frequency.
- there are still “species” in asexual organisms, i.e. clusters in genotype space. Genes that jump to another cluster (a human pathogen → a soil bacteria) can certainly have a wildly different effect on that new cluster/species (there is something like reproductive isolation for asexual species with horizontal gene transfer).
- the diploidy and genotypic/phenotypic complexity of sexual reproducing organisms makes them much more robust to mutations. I’m not sure why you think a single nucleotide mutation can’t have a massive effect on a bacteria. They have less genes and less phenotypes but the map is still incredibly intricate and continent.
Hope this helps.
I like it—added here as Schwarz’s Law (you gotta have more than one for this to be the first :) https://www.secretorum.life/p/the-grand-encyclopedia-of-eponymous