A Modified Model of Segregation Distortion in DROSOPHILA MELANOGASTER.
A Modified Model of Segregation Distortion in DROSOPHILA MELANOGASTER.
复制标题
果蝇分离畸变的改进模型。
作者：
Y. Hiraizumi;Diana W. Martin;Irene A. Eckstrand
本文分析了黑腹果蝇（Drosophilamelanogaster）偏分离（SegregationDistorter，SD）系统的元件Sd和Rsp，并建立了以下几点：（1）我们的观察结果支持Martin和Hiraizumi（1979）提出的Rsp（s）位点的多等位基因模型。(2)SD的修饰语，暂时用符号M（SD）表示，被发现接近于cn（2 R-57.5）。(3)在特定的基因型条件下，Sd杂合子雄性几乎完全不育。基于这些观察结果，提出了以下分离畸变的修正模型：（1）M（SD）基因座产生多聚体阻遏蛋白，其结合到Rsp基因座作为正常精子发生的必要条件。M（SD）纯合子产生阻遏物M（SD）/M（SD）;而其正常等位基因M（+）（SD）的纯合子产生M（+）（SD）/M（+）（SD）阻遏物。M（SD）/M（+）（SD）杂合子产生M（SD）/M（+）（SD）阻遏物。(2)Sd基因座产生某种产物，类似于大肠杆菌乳糖系统中的诱导物。大肠杆菌中，倾向于结合与Rsp基因座复合的阻遏物。这种结合破坏了阻遏物-Rsp复合物，导致Rsp位点被打开，Rsp转录产物反过来导致精子功能障碍。(3)Rsp（i）是Rsp的一个等位基因，它与阻遏物具有很强的络合亲和力，因此Rsp（i）-阻遏物复合物对Sd产物的诱导活性具有“抗性”。另一方面，Rsp（s）具有比Rsp（i）更弱的络合亲和力，并且亲和力的程度在不同的Rsp（s）等位基因之间变化。上述模型的一个可能的扩展进行了讨论。
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.