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Gene Review

xol-1  -  Protein XOL-1

Caenorhabditis elegans

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Disease relevance of xol-1

  • 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 [1].

High impact information on xol-1

  • 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 [2].
  • 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 [2].
  • In xol-1 mutant XO embryos that activate the XX mode of dosage compensation and die from inappropriately low X chromosome transcript levels, DPY-27 becomes localized to X [3].
  • The other uses the putative RNA-binding protein encoded by fox-1 to reduce the level of xol-1 protein [4].
  • We demonstrate that the dose-sensitive signal elements on chromosome X control xol-1 through two different molecular mechanisms [4].

Biological context of xol-1

  • XO-specific lethality most likely results from the reduction in X chromosome expression caused by xol-1 mutations [1].
  • Specific genes termed X-signal elements, which are present on the X chromosome, act in a concerted dose-dependent fashion to regulate levels of the developmental switch gene xol-1 [5].
  • Twenty-three mutations were isolated after chemical mutagenesis and found to fall into both expected classes (four dominant tra-1 mutations and eight recessive xol-1 mutations) and novel classes [6].

Regulatory relationships of xol-1

  • Here we show the signal includes discrete, trans-acting autosomal signal elements (ASEs) that counter XSEs to coordinately control both sex determination and dosage compensation. sea-1, the first autosomal signal element, encodes a T-box transcription factor that opposes XSEs by activating transcription of xol-1 [7].

Other interactions of xol-1

  • Additionally, fox-1(Delta) impairs male mating efficiency, which, we propose, represents another function of fox-1, independent of xol-1 and its role in sex determination [8].
  • In XX hermaphrodites, accumulation of both her-1 transcripts is repressed by the sdc genes, which in turn are negatively regulated by the xol-1 gene [9].


  1. 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. Cell (1988) [Pubmed]
  2. xol-1 acts as an early switch in the C. elegans male/hermaphrodite decision. Rhind, N.R., Miller, L.M., Kopczynski, J.B., Meyer, B.J. Cell (1995) [Pubmed]
  3. DPY-27:a chromosome condensation protein homolog that regulates C. elegans dosage compensation through association with the X chromosome. Chuang, P.T., Albertson, D.G., Meyer, B.J. Cell (1994) [Pubmed]
  4. X-chromosome-counting mechanisms that determine nematode sex. Nicoll, M., Akerib, C.C., Meyer, B.J. Nature (1997) [Pubmed]
  5. XOL-1, primary determinant of sexual fate in C. elegans, is a GHMP kinase family member and a structural prototype for a class of developmental regulators. Luz, J.G., Hassig, C.A., Pickle, C., Godzik, A., Meyer, B.J., Wilson, I.A. Genes Dev. (2003) [Pubmed]
  6. Isolation of dominant XO-feminizing mutations in Caenorhabditis elegans: new regulatory tra alleles and an X chromosome duplication with implications for primary sex determination. Hodgkin, J., Albertson, D.G. Genetics (1995) [Pubmed]
  7. The T-box transcription factor SEA-1 is an autosomal element of the X:A signal that determines C. elegans sex. Powell, J.R., Jow, M.M., Meyer, B.J. Dev. Cell (2005) [Pubmed]
  8. Genetic and molecular analysis of fox-1, a numerator element involved in Caenorhabditis elegans primary sex determination. Skipper, M., Milne, C.A., Hodgkin, J. Genetics (1999) [Pubmed]
  9. Evidence for multiple promoter elements orchestrating male-specific regulation of the her-1 gene in Caenorhabditis elegans. Li, W., Streit, A., Robertson, B., Wood, W.B. Genetics (1999) [Pubmed]
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