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The scute (T4) gene acts as a numerator element of the X:a signal that determines the state of activity of sex-lethal in Drosophila.

1989; Springer Nature; Volume: 8; Issue: 10 Linguagem: Inglês

10.1002/j.1460-2075.1989.tb08459.x

1460-2075

Miguel Torres, Lucas Sánchez,

Developmental Biology and Gene Regulation

Research Article1 October 1989free access The scute (T4) gene acts as a numerator element of the X:a signal that determines the state of activity of sex-lethal in Drosophila. M. Torres M. Torres Centro de Investigaciones Biológicas, Madrid, Spain. Search for more papers by this author L. Sánchez L. Sánchez Centro de Investigaciones Biológicas, Madrid, Spain. Search for more papers by this author M. Torres M. Torres Centro de Investigaciones Biológicas, Madrid, Spain. Search for more papers by this author L. Sánchez L. Sánchez Centro de Investigaciones Biológicas, Madrid, Spain. Search for more papers by this author Author Information M. Torres1 and L. Sánchez1 1Centro de Investigaciones Biológicas, Madrid, Spain. The EMBO Journal (1989)8:3079-3086https://doi.org/10.1002/j.1460-2075.1989.tb08459.x PDFDownload PDF of article text and main figures. ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinked InMendeleyWechatReddit Figures & Info The ratio of X chromosomes to sets of autosomes (X:A) is the primary genetic signal that determines sex and dosage compensation in Drosophila. The gene Sex-lethal (Sxl) receives this signal and is responsible for the execution of the alternative developmental programmes of males and females. We have found that the scute (T4) gene, which is involved in neurogenesis, also plays a role in the activation of Sxl. The following results suggest that scute (T4) may be a numerator element of the X:A signal: scute (T4) mutations show female-specific lethality. There are female-specific lethal synergistic interactions between sis-a, a previously described numerator element, and mutants for T4. The female lethality is suppressed by SxlM1, a constitutive allele which expresses an active Sxl product independently of the X:A ratio. The Hw685 mutation, which overexpresses T4, is lethal to males with a duplication of sis-a. This lethality is suppressed by either Sxlf1, or the T4 point mutation sc10-1. There are female-specific lethal interactions between sc10-1 and daughter-less (da), a gene needed maternally for Sxl to become active. The sc10-1 mutation masculinizes triploid intersexes. Previous ArticleNext Article Volume 8Issue 101 October 1989In this issue RelatedDetailsLoading ...