Cline T W
Genetics. 1978 Dec;90(4):683-98. doi: 10.1093/genetics/90.4.683.
A new spontaneous mutation named Sex-lethal, Male-specific No. 1 (SxlM1) is described that is lethal to males, even in the presence of an Sxl+ duplication. Females homozygous for SxlM1 are fully viable. This dominant, male-specific lethal mutation is on the X chromosome approximately 0.007 map units to the right of a previously isolated female-specific mutation, Female-lethal, here renamed Sex-lethal, Female-specific No. 1 (SxlF1). SxlM1 and SxlF1 are opposite in nearly every repect, particularly with regard to their interaction with maternal effect of the autosomal mutation, daughterless (da). Females that are homozygous for da produce defective eggs that cannot support female (XX) development. A single dose of SxlM1 enables daughters to survive this da female-specific lethal maternal effect. A duplication of the Sxl locus weakly mimics this action of SxlM1. In contrast, SxlF1 and a deficiency for Sxl, strongly enhance the female-lethal effects of da. The actions of SxlM1 and SxlF1 are explained by a model in which expression of the Sxl locus is essential for females, lethal for males, and under the control of a product of the da locus. It is suggested that SxlM1 is a constitutive mutation at the Sxl locus.
描述了一种名为性致死,雄性特异性1号(SxlM1)的新自发突变,该突变对雄性具有致死性,即使存在Sxl +重复也是如此。SxlM1纯合的雌性完全可行。这种显性的、雄性特异性致死突变位于X染色体上,在先前分离的雌性特异性突变——雌性致死(此处重新命名为性致死,雌性特异性1号,SxlF1)右侧约0.007个图距单位处。SxlM1和SxlF1在几乎每个方面都相反,特别是在它们与常染色体突变无女儿(da)的母体效应的相互作用方面。da纯合的雌性产生有缺陷的卵,不能支持雌性(XX)发育。单剂量的SxlM1能使女儿在这种da雌性特异性致死母体效应中存活。Sxl基因座的重复微弱地模拟了SxlM1的这种作用。相比之下,SxlF1和Sxl的缺失强烈增强了da的雌性致死效应。SxlM1和SxlF1的作用由一个模型解释,在该模型中,Sxl基因座的表达对雌性至关重要,对雄性具有致死性,并且受da基因座产物的控制。有人认为SxlM1是Sxl基因座的组成型突变。