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xol-1: a gene that controls the male modes of both sex determination and X chromosome dosage compensation in C. elegans.
Miller, L M; Plenefisch, J D; Casson, L P; Meyer, B J.
Afiliação
  • Miller LM; Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.
Cell ; 55(1): 167-83, 1988 Oct 07.
Article em En | MEDLINE | ID: mdl-3167975
ABSTRACT
Loss-of-function mutations in the X-linked gene xol-1 cause the feminization and death of XO animals (normally males) by shifting the sex determination and dosage compensation pathways toward their hermaphrodite modes. XO-specific lethality most likely results from the reduction in X chromosome expression caused by xol-1 mutations. Mutations in genes required for the hermaphrodite mode of dosage compensation suppress lethality but not feminization, and restore X chromosome expression to nearly wild-type levels. Mutations in genes that control the hermaphrodite modes of both sex determination and dosage compensation fully suppress both defects. These interactions suggest that xol-1 is the earliest-acting gene in the known hierarchy controlling the male/hermaphrodite decision and is perhaps the gene nearest the primary sex-determining signal. We propose that the wild-type xol-1 gene product promotes male development by ensuring that genes (or gene products) directing hermaphrodite sex determination and dosage compensation are inactive in XO animals. Interestingly, in addition to feminizing XO animals, xol-1 mutations further masculinize XX animals already partially masculinized.
Assuntos
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Análise para Determinação do Sexo / Caenorhabditis / Mecanismo Genético de Compensação de Dose Limite: Animals Idioma: En Revista: Cell Ano de publicação: 1988 Tipo de documento: Article
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Análise para Determinação do Sexo / Caenorhabditis / Mecanismo Genético de Compensação de Dose Limite: Animals Idioma: En Revista: Cell Ano de publicação: 1988 Tipo de documento: Article