Why don’t female organisms insert more of their own DNA into the offspring?
I don’t think Fisher’s principle explains it, because it only applies to the level of which sex your offspring has, and there’s a clear advantage of having a male offspring when there’s many females around.
But if you’re female, and sperm and egg mix, you could theoretically control how much of the male’s DNA gets to contribute to the embryo. And there’s not much to stop you, since the male can’t check beforehand how much of its DNA you will use. But if a gene causes the female organism to increase more of its DNA into the offspring, that gene also increases its own chance of continuing to exist.
Sure, the offspring will be less fit on average, but I’m astonished that the equilibrium is that the female organism doesn’t “cheat” at all, instead of there being a 2⁄3 female 1⁄3 male offspring genome or something.
Maybe this is a situation where every gene benefits by not cheating, but individual genes defecting would make sense? And if so, how does the reproductive process prevent this?
It’s worth starting by noting, that male and female births are not 50-50. While conceptions are 50-50, births aren’t and there are mechanisms that terminate pregnancies unsuccessfully that have different likelihoods based on gender.
While it makes sense that the value is near 50% for humans it’s not exactly both in reality and in computer models I did for human evolution (and it surprised me).
Sexual selection is very useful. In humans, mitochondrial DNA is only passed maternally and we see that evolution reduced the number of mitochondrial genes to a minimum.
For each of the chromosomes we get one from our mother and one from our father. There’s no easy way to give 1.25 from the mother and 0.75 from the father. If we get two of one of the chromosomes or none from one parent in most cases the pregnancy terminates unsuccessfully and in the few remaining cases, it produces severe harm (like down syndrome).
What asymmetries did you introduce into your simulations that lead to a difference? Models with no gender differences but with mandatory sexual reproduction usually tend to be 50⁄50 in my experience.
My models had humans with their full 46 chromosomes and multiple genes per chromosome. In addition, I have transposons on those chromosomes. I also tried to have a model of mating behavior where males and females obviously have different roles.
Mutations on the x-chromosome lead more frequently to pregnancy termination in male offspring. This is pretty obvious given that female offspring have more redundancy when it comes to the X chromosome.
The transposon-related pregnancy terminations that in turn terminate more female pregnancies than male ones are less obvious. I think I have some insight there that could be publishable. If anyone wants to collaborate on a paper I’m happy to say more privately.
Transposons and their effects get often not taken as seriously as they should.
I think this makes sense because eggs are haploid (already only have 23 chromosomes) but a natural next question is: why are eggs haploid if there is a major incentive to pass more of the 46 chromosomes?
I think the biggest reason why you don’t commonly see the selective incorporation of male DNA is because the machinery to do the selection would be too costly compared to just transitioning to asexual reproduction.
That being said, there’s a wide breadth of parthenogenesis strategies, of which the most relevant are the kleptons, which can sometimes incorporate some of the male DNA.
Individual genes defecting are probably closest to transposons and other selfish genetic elements, and those are in competition with systems that silence them to prevent them from defecting.
Polyploidy probably have greater flexibility for the non-balanced incorporation of DNA, but I’m not familiar enough to comment any more.
From another message:
I guess selective incorporation machinery might not be too costly, but why selectively incorporate when you can just turn to full asexual reproduction, or have both sexual and asexual reproduction? (ie: virgin birth in sharks, some reptiles, etc.)
I guess it’s the difference between having each offspring being an 90⁄10 split of genetics, or having 80% of your population asexually reproduce and 20% sexually reproduce.
Why don’t female organisms insert more of their own DNA into the offspring?
I don’t think Fisher’s principle explains it, because it only applies to the level of which sex your offspring has, and there’s a clear advantage of having a male offspring when there’s many females around.
But if you’re female, and sperm and egg mix, you could theoretically control how much of the male’s DNA gets to contribute to the embryo. And there’s not much to stop you, since the male can’t check beforehand how much of its DNA you will use. But if a gene causes the female organism to increase more of its DNA into the offspring, that gene also increases its own chance of continuing to exist.
Sure, the offspring will be less fit on average, but I’m astonished that the equilibrium is that the female organism doesn’t “cheat” at all, instead of there being a 2⁄3 female 1⁄3 male offspring genome or something.
Maybe this is a situation where every gene benefits by not cheating, but individual genes defecting would make sense? And if so, how does the reproductive process prevent this?
It’s worth starting by noting, that male and female births are not 50-50. While conceptions are 50-50, births aren’t and there are mechanisms that terminate pregnancies unsuccessfully that have different likelihoods based on gender.
While it makes sense that the value is near 50% for humans it’s not exactly both in reality and in computer models I did for human evolution (and it surprised me).
Sexual selection is very useful. In humans, mitochondrial DNA is only passed maternally and we see that evolution reduced the number of mitochondrial genes to a minimum.
For each of the chromosomes we get one from our mother and one from our father. There’s no easy way to give 1.25 from the mother and 0.75 from the father. If we get two of one of the chromosomes or none from one parent in most cases the pregnancy terminates unsuccessfully and in the few remaining cases, it produces severe harm (like down syndrome).
What asymmetries did you introduce into your simulations that lead to a difference? Models with no gender differences but with mandatory sexual reproduction usually tend to be 50⁄50 in my experience.
My models had humans with their full 46 chromosomes and multiple genes per chromosome. In addition, I have transposons on those chromosomes. I also tried to have a model of mating behavior where males and females obviously have different roles.
Mutations on the x-chromosome lead more frequently to pregnancy termination in male offspring. This is pretty obvious given that female offspring have more redundancy when it comes to the X chromosome.
The transposon-related pregnancy terminations that in turn terminate more female pregnancies than male ones are less obvious. I think I have some insight there that could be publishable. If anyone wants to collaborate on a paper I’m happy to say more privately.
Transposons and their effects get often not taken as seriously as they should.
I think this makes sense because eggs are haploid (already only have 23 chromosomes) but a natural next question is: why are eggs haploid if there is a major incentive to pass more of the 46 chromosomes?
If you would say that there are two copies of chromosome 11 in the egg and none in sperm, you would lose sexual selection for chromosome 11.
From a message on reddit by /u/eniteris:
From another message:
(I am satisfied with this as an explanation)
To put it another way, if a female inserts more of her DNA into an offspring then she loses out on the benefits of sexual reproduction.
It’s not clear this is the case when the sum isn’t 1. (i.e. 1⁄2 + 1⁄2 = 1, versus 1⁄2 + 1 = 3/2*)
*I’m guessing that’s the breakdown.