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Gene Review

woc  -  without children

Drosophila melanogaster

Synonyms: CG5965, Dmel\CG5965, WOC, Woc
 
 
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Disease relevance of woc

 

High impact information on woc

  • The woc gene, located in polytene chromosomal region 97F, consists of 11 exons [1].
  • Unlike ring glands from wild-type D. melanogaster larvae, glands from woc mutants cannot convert radiolabelled C or 25-hydroxycholesterol (25C) to 7dC or 7-dehydro-25-hydroxycholesterol (7d25C) in vitro, nor to ecdysone (E) [2].
  • The first step in ecdysteroidogenesis, i.e. the 7,8-dehydrogenation of dietary cholesterol (C) to 7-dehydrocholesterol (7dC), is blocked in Drosophila melanogaster homozygous woc (without children) third instar larval ring glands (source of ecdysone) [2].
  • Data previously reported (Wismar et al., 2000) indicate that the woc gene encodes a zinc-finger protein that apparently modulates the activity of the 7,8-dehydrogenase [2].
  • The composite data suggest that the woc gene may regulate 20E-dependent alpha-tubulin detyrosination and that microtubules may be involved in sterol transport and sterol utilization in insect [3].
 

Associations of woc with chemical compounds

  • Although a 6.8-kb woc gene transcript encoding a 187-kDa potential transcription factor has been cloned and lack of a specific cholesterol 7,8-dehydrogenease that mediates the first step in the ecdysteroidogenic pathway is likely the cause for ecdysteroid deficiency, the cellular events controlled by the woc gene remain unclear [3].
 

Other interactions of woc

  • In the present study, we investigated the effect of the woc gene mutation on the expression and tyrosination of alpha-tubulin in the woc(rgl) mutant [3].
 

Analytical, diagnostic and therapeutic context of woc

  • Oral administration of 7dC, but not C, results in a dramatic increase in ecdysteroid production both in vivo and in vitro by the woc mutant brain-ring gland complexes and affects a partial rescue to the beginning of pupal-adult development, but no further, despite elevated whole-body ecdysteroid titers [2].

References

  1. The mutation without children(rgl) causes ecdysteroid deficiency in third-instar larvae of Drosophila melanogaster. Wismar, J., Habtemichael, N., Warren, J.T., Dai, J.D., Gilbert, L.I., Gateff, E. Dev. Biol. (2000) [Pubmed]
  2. Woc (without children) gene control of ecdysone biosynthesis in Drosophila melanogaster. Warren, J.T., Wismar, J., Subrahmanyam, B., Gilbert, L.I. Mol. Cell. Endocrinol. (2001) [Pubmed]
  3. Woc gene mutation causes 20E-dependent alpha-tubulin detyrosination in Drosophila melanogaster. Jin, X., Sun, X., Song, Q. Arch. Insect Biochem. Physiol. (2005) [Pubmed]
 
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