Hiraizumi Y
Department of Zoology, University of Texas, Austin 78712.
Genetics. 1990 Jul;125(3):515-25. doi: 10.1093/genetics/125.3.515.
Current models of segregation distortion based on previous experimental results predict that, in the Sd heterozygous Rspi/Rsps male, the chromosome carrying the sensitive Rsps allele is distorted or transmitted in a frequency smaller than that of the expected Mendelian 0.5 relative to the chromosome carrying the insensitive Rspi allele. The present study presents a case where this does not occur, that is, when the genotype of the males is supp-X(SD)/Y; Sd E(SD)Rspi M(SD)+/Sd+ E(SD)+ Rsps M(SD)+ where supp-X(SD) is an X chromosome carrying a strong suppressor or suppressors of SD activity and SD+ E(SD)+ Rsps M(SD)+ is the standard cn bw chromosome. Following the "inseminated female transfer" procedure, young males of the above genotype carrying the standard-X instead of the supp-X(SD) chromosome show k values for the SD chromosome (frequencies of the SD chromosome recovered among progeny) of about 0.75, but with the supp-X(SD) chromosome, the k values are reduced to 0.36-0.41. Several possibilities other than the mechanism of segregation distortion to explain the reduced k values are ruled out. The occurrence of "negative segregation distortion" is clearly demonstrated, where the chromosome carrying the Rspi allele is distorted but the chromosome with the Rsps allele is not. This result requires a major modification of the current models or even a new model for the mechanism of segregation distortion to accommodate Rsp allele sensitivity or insensitivity. The present study also shows that males of the genotype, Sd Rspss M(SD)+/Sd+ Rspss M(SD), are almost completely sterile, but their fertility is considerably increased when SD activity is suppressed by the presence of the supp-X(SD) chromosome. This result suggests that the amount of the Sd product is not limited with respect to the interacting sites available, that is, the amount is large enough to interact with both of the Rspss alleles.
基于先前实验结果的当前分离畸变模型预测,在Sd杂合的Rspi/Rsps雄性中,携带敏感Rsps等位基因的染色体相对于携带不敏感Rspi等位基因的染色体发生畸变或传递频率低于预期的孟德尔频率0.5。本研究呈现了一种并非如此的情况,即当雄性的基因型为supp-X(SD)/Y; Sd E(SD)Rspi M(SD)+/Sd+ E(SD)+ Rsps M(SD)+时,其中supp-X(SD)是携带一个或多个强SD活性抑制因子的X染色体,而SD+ E(SD)+ Rsps M(SD)+是标准的cn bw染色体。遵循“授精雌蝇转移”程序,上述基因型的年轻雄性若携带标准X染色体而非supp-X(SD)染色体,其SD染色体的k值(后代中回收的SD染色体频率)约为0.75,但携带supp-X(SD)染色体时,k值降至0.36 - 0.41。排除了除分离畸变机制之外的几种解释k值降低的可能性。明确证明了“负向分离畸变”的发生,即携带Rspi等位基因的染色体发生畸变,而携带Rsps等位基因的染色体未畸变。这一结果需要对当前模型进行重大修改,甚至需要一个新的分离畸变机制模型来适应Rsp等位基因的敏感性或不敏感性。本研究还表明,基因型为Sd Rspss M(SD)+/Sd+ Rspss M(SD)的雄性几乎完全不育,但当supp-X(SD)染色体的存在抑制SD活性时,其育性显著提高。这一结果表明,相对于可用的相互作用位点,Sd产物的量不受限制,即该量足够大以与两个Rspss等位基因相互作用。