Meiotic drive is a type of intragenomic conflict, whereby one or more loci within a genome will affect a manipulation of the meiotic process in such a way as to favor the transmission of one or more alleles over another, regardless of its phenotypic expression. More simply, meiotic drive is when one copy of a gene is passed on to offspring more than the expected 50% of the time. According to Buckler et al., "Meiotic drive is the subversion of meiosis so that particular genes are preferentially transmitted to the progeny. Meiotic drive generally causes the preferential segregation of small regions of the genome".
Meiotic drive in plants
The first report of meiotic drive came from Marcus Rhoades who in 1942 observed a violation of mendelian segregation ratios for the R locus - a gene controlling the production of the purple pigment anthocyanin in maize kernels - in a maize line carrying abnormal chromosome 10. This violation of mendelian segregation was later shown to be the result of an array of Kindr genes at present on the end of chromosome 10 which induce neocentromere activity in maize knobs, causing copies of maize chromosomes carrying knobs to preferentially reach the egg cell during female meiosis.
Meiotic drive in animals
Meiotic drive genes in animals have primarily been found in rodents and flies.
Meiotic drive in mice
A study by John Didion and Fernando Pardo-Manuel de Villena found evidence of a gene in mice (r2d2 – responder to meiotic drive 2) that is passed on more than 50% of the time. Gregor Mendel's First and Second Laws (the law of segregation and the law of independent assortment) tell us that there is a random chance of each allele being passed on to offspring, but selfish genes seem to break these laws.
Meiotic drive in flies
Selfish chromosomes of stalk-eyed flies have had ecological consequences. Driving X chromosomes lead to reductions in male fecundity, leading to frequency dependent selection maintaining both the driving alleles and wild-type alleles.
Multiple species of fruit fly are known to have driving X chromosomes, of which the best-characterized are found in Drosophila simulans. Three independent driving X chromosomes are known in D. simulans, called Paris, Durham, and Winters. In Paris, the driving gene encodes a DNA modelling protein ("heterochromatin protein 1 D2" or HP1D2), where the allele of the driving copy fails to prepare the male Y chromosome for meiosis. In Winters, the gene responsible ("Distorter on the X" or Dox) has been identified, though the mechanism by which it acts is still unknown. The strong selective pressure imposed by these driving X chromosomes has given rise to suppressors of drive, of which the genes are somewhat known for Winters, Durham, and Paris. These suppressors encode hairpin RNAs which match the sequence of driver genes (such as Dox), leading host RNA interference pathways to degrade Dox sequence. Autosomal suppressors of drive are known in Drosophila mediopunctata, Drosophila paramelanica, Drosophila quinaria, and Drosophila testacea, emphasizing the importance of these drive systems in natural populations.
It has been postulated that meiotic drivers could play a major role in speciation. For instance, the proposal that hybrid sterility (Haldane's rule) may arise from the divergent evolution of sex chromosome drivers and their suppressors.
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