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A MODIFIED MODEL OF SEGREGATION DISTORTION IN DROSOPHILA MELANOGASTER
Yuichiro Hiraizumi 1, Diana W. Martin 1, and Irene A. Eckstrand 1
1 Department of Zoology, The University of Texas at Austin, Texas 78712
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 Rsps 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) Rspi, an allele of Rsp, has a strong complexing affinity with the repressor such that the Rspi-repressor complex is "resistant" to the inducing activity of Sd product. Rsps, on the other hand, has a weaker complexing affinity than that of Rspi, and the degree of affinity varies among different Rsps alleles.—A possible extension of the above model is discussed.
Submitted on November 17, 1979Revised on March 4, 1980
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