Abstract
xol-1 is the earliest-acting gene in the known hierarchy that controls C. elegans sex determination and dosage compensation. We show that the primary sex-determining signal (the X/A ratio) directs the choice of sexual fate by regulating xol-1 transcript levels: high xol-1 expression during gastrulation triggers male development, whereas low expression at that time permits hermaphrodite development. Inappropriately high xol-1 expression causes hermaphrodites to activate the male program of development and die from a disruption in dosage compensation. These results demonstrate that xol-1 functions as an early developmental switch to set the choice of sexual fate and suggest that assessment of the X/A ratio occurs only early in embryogenesis to determine sex. Moreover, sdc-2, a gene that must be repressed by xol-1 to ensure male development, may be a direct target of negative regulation by xol-1.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Alternative Splicing
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Amino Acid Sequence
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Animals
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Caenorhabditis elegans / embryology
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Caenorhabditis elegans / genetics*
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Caenorhabditis elegans Proteins*
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Cloning, Molecular
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Disorders of Sex Development / genetics
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Dosage Compensation, Genetic
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Embryo, Nonmammalian / metabolism
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Gastrula / metabolism
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Gene Expression Regulation, Developmental*
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Genes, Helminth*
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Helminth Proteins / chemistry
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Helminth Proteins / genetics*
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Helminth Proteins / physiology
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Male
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Molecular Sequence Data
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Mutagenesis, Site-Directed
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RNA, Helminth / genetics
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RNA, Helminth / metabolism
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Recombinant Fusion Proteins / biosynthesis
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Sex Determination Analysis*
Substances
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Caenorhabditis elegans Proteins
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Helminth Proteins
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RNA, Helminth
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RNA, Messenger
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Recombinant Fusion Proteins
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XOL-1 protein, C elegans