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Gene Review

fem-3  -  Protein FEM-3

Caenorhabditis elegans

 
 
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Disease relevance of fem-3

  • Mutations in fem-3 resemble alleles of fem-1 (previously characterized): putative null alleles result in complete feminization of XX and XO animals, transforming them into fertile females [1].
 

High impact information on fem-3

  • In adult hermaphrodites (which are producing oocytes), most fem-3 RNA is found in the germ line, consistent with both the requirement for fem-3 in hermaphrodite spermatogenesis and the maternal effects of fem-3 on embryonic sex determination [2].
  • Whereas loss-of-function mutants in fem-3 produce only oocytes, hermaphrodites carrying any of nine fem-3 gain-of-function (gf) mutations make none; instead sperm are produced continuously and in vast excess over wild-type amounts [2].
  • Expression of fem-3 in the hermaphrodite germ line directs spermatogenesis and must be negatively regulated to allow the switch to oogenesis [2].
  • There is no increase in the steady-state level of fem-3(gf) RNA over wild-type, but there is an increase in the polyadenylation of fem-3(gf) RNA that is coincident with the unregulated fem-3 activity [2].
  • Male sexual development in the nematode Caenorhabditis elegans requires the genes fem-1, fem-2, and fem-3 [3].
 

Biological context of fem-3

  • We employed RNA interference to show that in all three species, the male-promoting function of fem-3 and its epistatic relationship with its female-promoting upstream repressor, tra-2, are conserved [4].
  • Both maternal and zygotic fem-3 activities are required for spermatogenesis in the XX hermaphrodite germline and for male development in somatic and germline tissues XO (male) animals [5].
  • Here we show that fem-3 RNA is contributed to embryos as a maternal product and that this RNA is degraded early in embryonic development [5].
  • The sequence of fem-3 predicts an open reading frame that could encode a soluble protein; putative fem-3 null mutants truncate this open reading frame [5].
  • Second, gld-1 mRNA is initially repressed by FBF (for fem-3 binding factor) to maintain stem cells but then becomes activated by the GLD-2 poly(A) polymerase once stem cells begin to make the transition into the meiotic cell cycle [6].
 

Anatomical context of fem-3

  • The finding of gain-of-function alleles which confer a phenotype opposite to that of loss-of-function alleles supports the idea that fem-3 plays a critical role in germ-line sex determination [7].
  • The decision to differentiate as a sperm or an oocyte is regulated by the sex-determining gene, fem-3 [2].
 

Regulatory relationships of fem-3

  • A loss of mog-1 might inappropriately activate fem-3 and thereby abolish the sperm/oocyte switch; its loss might also lead to misregulation of maternal RNAs and thus embryonic death [8].
 

Other interactions of fem-3

  • In Caenorhabditis elegans, fem-1, fem-2, and fem-3 play pivotal roles in sex determination [9].
  • While the masculinization is blocked by mutations in sex determining genes required for male development (her-1 and fem-3), the lethality, dumpiness and overexpression of X-linked genes are not, indicating that the effect of sdc-2 mutations on sex determination and dosage compensation are ultimately implemented by two independent pathways [10].
  • Previous work showed that at least six mog genes are required for repression by the fem-3 3' untranslated region, and that one of those genes, mog-1, encodes a DEAH-box protein [11].
  • The switch from spermatogenesis to oogenesis in the Caenorhabditis elegans hermaphrodite requires mog-6, which post-transcriptionally represses the fem-3 RNA [12].
 

Analytical, diagnostic and therapeutic context of fem-3

  • Results of a titration experiment support the hypothesis that a regulatory factor may bind the fem-3 3' UTR [2].
  • Molecular cloning and transcript analysis of fem-3, a sex-determination gene in Caenorhabditis elegans [13].
  • However, additional data, including Southern blot analyses on 48 of the strains, indicated that most of the UV radiation-induced fem-3 mutations were not deficiencies, as originally inferred from their homozygous inviability [14].

References

  1. Sex determination in the nematode C. elegans: analysis of tra-3 suppressors and characterization of fem genes. Hodgkin, J. Genetics (1986) [Pubmed]
  2. Control of the sperm-oocyte switch in Caenorhabditis elegans hermaphrodites by the fem-3 3' untranslated region. Ahringer, J., Kimble, J. Nature (1991) [Pubmed]
  3. Caenorhabditis elegans sex-determining protein FEM-2 is a protein phosphatase that promotes male development and interacts directly with FEM-3. Chin-Sang, I.D., Spence, A.M. Genes Dev. (1996) [Pubmed]
  4. Rapid coevolution of the nematode sex-determining genes fem-3 and tra-2. Haag, E.S., Wang, S., Kimble, J. Curr. Biol. (2002) [Pubmed]
  5. The Caenorhabditis elegans sex determining gene fem-3 is regulated post-transcriptionally. Ahringer, J., Rosenquist, T.A., Lawson, D.N., Kimble, J. EMBO J. (1992) [Pubmed]
  6. The GLD-2 poly(A) polymerase activates gld-1 mRNA in the Caenorhabditis elegans germ line. Suh, N., Jedamzik, B., Eckmann, C.R., Wickens, M., Kimble, J. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  7. Gain-of-function mutations of fem-3, a sex-determination gene in Caenorhabditis elegans. Barton, M.K., Schedl, T.B., Kimble, J. Genetics (1987) [Pubmed]
  8. The mog-1 gene is required for the switch from spermatogenesis to oogenesis in Caenorhabditis elegans. Graham, P.L., Kimble, J. Genetics (1993) [Pubmed]
  9. The Caenorhabditis elegans sex-determining protein FEM-2 and its human homologue, hFEM-2, are Ca2+/calmodulin-dependent protein kinase phosphatases that promote apoptosis. Tan, K.M., Chan, S.L., Tan, K.O., Yu, V.C. J. Biol. Chem. (2001) [Pubmed]
  10. The Caenorhabditis elegans gene sdc-2 controls sex determination and dosage compensation in XX animals. Nusbaum, C., Meyer, B.J. Genetics (1989) [Pubmed]
  11. The hermaphrodite sperm/oocyte switch requires the Caenorhabditis elegans homologs of PRP2 and PRP22. Puoti, A., Kimble, J. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  12. Roles of the C. elegans cyclophilin-like protein MOG-6 in MEP-1 binding and germline fates. Belfiore, M., Pugnale, P., Saudan, Z., Puoti, A. Development (2004) [Pubmed]
  13. Molecular cloning and transcript analysis of fem-3, a sex-determination gene in Caenorhabditis elegans. Rosenquist, T.A., Kimble, J. Genes Dev. (1988) [Pubmed]
  14. Genetic and molecular analyses of UV radiation-induced mutations in the fem-3 gene of Caenorhabditis elegans. Hartman, P.S., De Wilde, D., Dwarakanath, V.N. Photochem. Photobiol. (1995) [Pubmed]
 
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