Woc gene mutation causes 20E-dependent alpha-tubulin detyrosination in Drosophila melanogaster.
The mutation without children(rgl) (woc(rgl)) is a newly described ecdysone-deficient Drosophila mutant. The woc(rgl) mutant larvae show developmental arrestment at the late larval stage and fail to form a puparium due to the failure of the ring gland to secret normal levels of ecdysone. 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. 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. Our results demonstrated that the mutation in the woc gene caused 20E-dependent alpha-tubulin detyrosination, but had no significant effect on the expression of total alpha- and beta-tubulin in the homozygous woc(rgl) mutant larvae. Immunocytochemical study revealed that 20E-induced alpha-tubulin detyrosination led to the diminishing of tyrosinated alpha-tubulin signals from microtubules, resulting in the disruption of microtubule structure. 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.[1]References
- 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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