Talk:Intragenomic conflict

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This page needs some cleaning up in grammar and style. Very often a colloquial tone is chosen.

Anyone got an idea how to rewrite this section? --> "Male-killing

Male embryos (in the case of cytoplasmic inherited bacteria) or male larvae (in the case of Microsporidia) are killed. It occurs in many insects. Unless the females that contain the cytoplasmic genes benefit from this there is no reason these genes might spread. In cases where a cytoplasmic element completely kills any males and the siblings are in close proximity, the aborted males are consumed by the females, which increases the females' chances of survival."

I gave a shot but don't have much more time right now.Lukas 03:31, 7 February 2006 (UTC)

Ok, I agree that the page needs some cleaning up in grammar and style. I just wrote it quickly to start the topic.

About the male-killing section, you must focus on the interest of the cytoplasmic genes that cause these phenotypic effects. A male is a dead-end for them. This excerpt is from the article from Nature Reviews Genetics from the references:

"Cytoplasmic incompatibility", induced y the cytoplasmically inherited bacterium Wolbachia (which is widespread in insects, arachnids (spiders), crustaceans and nematodes), also involves a modification-rescue system. However, in this case, uninfected zygotes are killed by a paternal effect from infected fathers, with a net increase in the frequency of infected individuals. In some cases, these elements [post-segregation distorters] spread through panmictic populations, whereas others requires structured populations or competition among siblings for resources (for example, Medea) for their spread. Cytoplasmic incompatibility, for instance, involves the death of uninfected individuals, but this only indirectly increases the frequency of the agent that induces the incompatibility and there is no direct benefit. Population size and structure are important in determining the ease of invasion and increase of these elements.

Waldow 20:03, 12 May 2006 (UTC)

I changed a few things regarding meiotic drive. First, cases of sex ratio biases caused by Y chromosome meiotic drive are rather controversial in humans, actually it has never been shown properly to my knowledge, contrary to insects, where many cases of Y or X sex-ratio drives are very well documented (see jaenike 2001, annual reviews of ecology ans systematics). I cited the X chromosome drive as an example (in Drosophila simulans and many others...). I also pointed out that some meiotic drive systems are caused by an exploitation of the asymmetry in meiosis (in females only) where only one product of meiosis becomes an egg and the other degenerate. Note that there is a controversy in names, because many authors suggest only those systems should be called meiotic drive, as they rely on a modification of the random process of meiosis, whereas the other cases take place after meiosis, and thus pertain to the general class of 'transmission ratio distorters'. I didn't emphasize on this controversy, though. Also I would like to stress that it should be more apparent in what meiotic drive is an example of intragenomic conflict, that is a situation in which several genes in the same genome compete. The reason is that a meiotic driver can invade a population despite having a potential cost for fitness, and thus can induce a general loss of fitness for all other loci. In the case of sex-ratio drive, the change in sex-ratio is in itself costly for autosomal genes : when there is an excess of females, an autosomal gene transmits itself better if the carrier produces more males, but the driver X provokes a still increasing female excess. I have plenty of references that can be added to this talk if someone is interested in having more feedback.

Selui 09:53, 13 July 2006 (UTC)