xol-1 acts as an early switch in the C. elegans male hermaphrodite decision
Article Abstract:
Experimental analysis of the function of xol-1 gene in dosage compensation and sex determination in Caenorhabditis elegans reveals that xol-1 serves as an early development switch to determine the choice of sexual fate in C. elegans. The primary sex-determining signal (X A ratio) modulates the xol-1 transcript levels to mediate the sexual fate selection. Low expression of xol-1 causes hermaphrodite development while high xol-1 expression activates male development. The sdc-2 gene that undergoes suppression by xol-1 functions as a target of negative xol-1 regulation.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1995
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Feedback control of sex determination by dosage compensation revealed through Caenohabditis elegans sdc-3 mutations
Article Abstract:
A new gene, sdc-3, that controls sex determination and dosage compensation in Caenorhabditis elegans was identified. Genetic analysis of the three classes of sdc-3 alleles showed that the two activities in the gene were separately mutable which implied that they function independently. Results also showed that disruption of dosage compensation affects the sexual fate through the suppression of sex determination defect. A feedback mechanism that regulates the sex determination pathaway was proposed to explain the self-suppression phenomenon.
Publication Name: Genetics
Subject: Biological sciences
ISSN: 0016-6731
Year: 1993
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Independent domains of the Sdc-3 protein control sex determination and dosage compensation in C. elegans
Article Abstract:
The Caenorhabditis elegans sdc-3 gene is an early-acting regulatory gene that controls both sex determination and dosage compensation. Sequence analysis of defined sdc-3 mutants showed that dosage compensation is controlled by a region in the Sdc-3 protein corresponding to a pair of zinc finger motifs. On the other hand, the sex determination function of Sdc-3 is controlled by a region exhibiting similarity to the ATP-binding domain of myosin.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1993
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