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TWO CLOSELY LINKED MUTATIONS IN <i>DROSOPHILA MELANOGASTER</i> THAT ARE LETHAL TO OPPOSITE SEXES AND INTERACT WITH DAUGHTERLESS
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1978
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CytogeneticsGeneticsMolecular GeneticsFemale Reproductive FunctionReproductive BiologyEpigeneticsEmbryologyFemale InfertilitySex DifferencesPublic HealthSomatic GeneticsNew Spontaneous MutationDevelopmental GeneticsMedicineGenetic VariationChromosomal RearrangementGene EvolutionPopulation GeneticsBiologyChromosome DynamicsDevelopmental BiologyGenetic DisorderEvolutionary BiologyMale-specific Lethal MutationGenetic MechanismChromosome BiologyEvolutionary Developmental BiologyDa Locus
Homozygous da mutants produce defective eggs that cannot support female (XX) development. The study describes a new spontaneous mutation, Sex‑lethal, Male‑specific #1 (SxlM1), which is lethal to males even with an Sxl + duplication. SxlM1 is a dominant, male‑specific lethal mutation located ~0.007 map units right of SxlF1 on the X chromosome, and its action is explained by a model where Sxl expression is essential for females, lethal for males, and regulated by a product of the da locus. SxlM1 homozygotes are fully viable, a single copy rescues daughters from the da maternal lethal effect, and the mutation appears constitutive, whereas SxlF1 and Sxl deficiency strongly enhance da’s female‑lethal effect, highlighting opposite interactions with da.
ABSTRACT A new spontaneous mutation named Sex-lethal, Male-specific #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 #1 (SxlF1). SxlM1 and SxlF1 are opposite in nearly every respect, particularly with regard to their interaction with the 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.