Is Stellate a relict meiotic driver?

Is Stellate a Relict Meiotic Driver? X 0 males of Drosophila melanogaster are sterile. Associated with this sterility is the presence of crystals in the sperm. Crystal production is determined by the Stellate (Ste) locus which maps to position 45.7 on the X chromosome (HARDY et al. 1984). Expression of stellate is repressed in normal males by Suppressor of Stellate Su(Ste) on the Y chromosome just proximal to the fertility factor kl-2 (LIVAK 1984, 1990). In D. simulans and D. mauritiana the Stellate sequence has been identified on the Y chromosome whereas in D. erecta, D. teissieri and D. yakuba it is not found at all. This is taken as an indication that the gene is possibly not necessary for normal spermatogenesis (LIVAK 1990). How could a gene which is possibly not required for spermatogenesis, and which can render the host sterile unless suppressed ever have evolved? Below I attempt to answer this question by proposing that Stellate was originally a meiotic drive gene. Consider a Drosophilid with " normal " meiosis in the male. The meiotic process involves accurate packing and winding of DNA. Consider now a mutant gene on the X which interferes with DNA packing in such a manner that the Y chromosome is more profoundly affected than the X. This might be simply due to the fact that the large Y has more DNA or hetero-chromatin requiring packing than the X or because the Y has more sites of interaction with the mutant protein. In consequence the gene will be present in more than 50% of the viable sperm. So long as the fertility of this fly is not reduced too dramatically this gene can invade. In contrast, a comparable gene on the Y would not be successful. Formally the gene is a X vs. Y meiotic driver. Interference with the packing of heterochromatin is believed to underlie the mechanism of drive in the Segregation Distorter system in Drosophila (Wu 1991). As the driver invades so it imposes a cost in both reducing male fertility and biasing the sex ratio. Thus a suppressor of this condition on the Y chromosome can also invade and go to a stable equilibrium (HURST and POMIANKOWSKI 1991). If this suppressor acts in a dose dependent fashion then a duplication of the driver locus can once again act as a driver by evading suppression. This driver can in turn however be …