If gene B only provides a benefit when gene A is already present, gene A must spread through a breeding population before gene B. And if gene A does not by itself provide a reproductive fitness advantage, it becomes nearly impossible for gene B to ever spread.
This seems to contrary to what I was taught in university ten years ago. At the time the thesis that there’s a lot of gene drift was the prevailing wisdom. What makes you think that it’s nearly impossible for a gene to win because of gene drift?
Thank you for pointing this out. I was aware of genetic drift, but I hadn’t read before that it accounted for the large majority of mutations.
I think what I was saying still largely holds true though: even if gene B has a neutral effect on reproductive fitness, the lack of fitness ADVANTAGE will mean that any spread that does occur will be by pure chance and is liable to being reversed by the same chance.
I actually don’t really know how to do the math on this one. If we start out with a population that all has the normal form of gene B and we the mutant form conveys no net reproductive fitness benefit or downside and the likelihood of each mutating into the other is equal, then I suppose we would expect the frequency of each variant to approach 50% given enough time.
Which makes me think that the likelihood of one allele spontaneously mutating into any other is probably pretty important. In fact I know of a specific disease in which the mutation from one allele to another in not symmetrical: Huntington’s disease.
Huntington’s disease is a codon repeat disorder, meaning that the mutant gene causing the disease has a codon that’s repeated at the end a large number of times. People with the disease have the letters ‘CAG’ repeated at the end of the gene at least 40 times. The more repetitions, the earlier the effects of the disease begin to show. There’s actually two villages in Venezuela (Barranquitas and Lagunetas) where children as young as ten acquire the disease due to having 70 or 80 CAG repeats.
I actually don’t really know how to do the math on this one. If we start out with a population that all has the normal form of gene B and we the mutant form conveys no net reproductive fitness benefit or downside and the likelihood of each mutating into the other is equal, then I suppose we would expect the frequency of each variant to approach 50% given enough time.
The relevant math would be Gambler’s ruin. If two forms have equal and independent chances of reproduction over a longer time-frame either of the forms will be wiped out.
But when it comes to the core of evolutionary theory, there isn’t even a good reason to try to do original research. There are plenty of professors in evolutionary theory that spend a lot of time investigating the issue, so unless you have good reason why the mainstream professors in evolutionary theory are wrong, it makes sense to default to the mainstream academic beliefs.
This seems to contrary to what I was taught in university ten years ago. At the time the thesis that there’s a lot of gene drift was the prevailing wisdom. What makes you think that it’s nearly impossible for a gene to win because of gene drift?
Thank you for pointing this out. I was aware of genetic drift, but I hadn’t read before that it accounted for the large majority of mutations.
I think what I was saying still largely holds true though: even if gene B has a neutral effect on reproductive fitness, the lack of fitness ADVANTAGE will mean that any spread that does occur will be by pure chance and is liable to being reversed by the same chance.
I actually don’t really know how to do the math on this one. If we start out with a population that all has the normal form of gene B and we the mutant form conveys no net reproductive fitness benefit or downside and the likelihood of each mutating into the other is equal, then I suppose we would expect the frequency of each variant to approach 50% given enough time.
Which makes me think that the likelihood of one allele spontaneously mutating into any other is probably pretty important. In fact I know of a specific disease in which the mutation from one allele to another in not symmetrical: Huntington’s disease.
Huntington’s disease is a codon repeat disorder, meaning that the mutant gene causing the disease has a codon that’s repeated at the end a large number of times. People with the disease have the letters ‘CAG’ repeated at the end of the gene at least 40 times. The more repetitions, the earlier the effects of the disease begin to show. There’s actually two villages in Venezuela (Barranquitas and Lagunetas) where children as young as ten acquire the disease due to having 70 or 80 CAG repeats.
The relevant math would be Gambler’s ruin. If two forms have equal and independent chances of reproduction over a longer time-frame either of the forms will be wiped out.
But when it comes to the core of evolutionary theory, there isn’t even a good reason to try to do original research. There are plenty of professors in evolutionary theory that spend a lot of time investigating the issue, so unless you have good reason why the mainstream professors in evolutionary theory are wrong, it makes sense to default to the mainstream academic beliefs.