A MODIFIED MODEL OF SEGREGATION DISTORTION IN DROSOPHILA MELANOGASTER

Abstract

Elements of the Segregation Distorter (SD) system of Drosophila melanogaster, Sd and Rsp, were analyzed and the following points were established: (1) The model of multiple alleles at the Rsp(s) locus proposed by Martin and Hiraizumi (1979) is supported by our observations. (2) A modifier of SD, tentatively symbolized M(SD), was found close to cn (2R-57.5). (3) Sd heterozygous males were found to show, under certain genotypic condition, almost complete sterility.-Based upon these observations, the following modified model of segregation distortion is proposed: (1) The M(SD) locus produces a multimeric repressor protein that binds to the Rsp locus as a necessary condition for normal spermiogenesis. M(SD) homozygotes produce a repressor M(SD)/M(SD); whereas, a homozygote for its normal allele M(+)(SD) produces a M(+)(SD)/M(+)(SD) repressor. M(SD)/M(+)(SD) heterzygotes produce a M(SD)/M(+)(SD) repressor. (2) The Sd locus produces a certain product that, like an inducer in the lactose system of E. coli, tends to bind with the repressor complexed with the Rsp locus. This binding disrupts the repressor-Rsp complex, causing Rsp locus to be turned on. The product of Rsp transcription, in turn, results in sperm dysfunction. (3) Rsp(i), an allele of Rsp, has a strong complexing affinity with the repressor such that the Rsp(i)-repressor complex is "resistant" to the inducing activity of Sd product. Rsp(s), on the other hand, has a weaker complexing affinity than that of Rsp(i), and the degree of affinity varies among different Rsp(s) alleles.-A possible extension of the above model is discussed.