Premium
woc gene mutation causes 20E‐dependent α‐tubulin detyrosination in Drosophila melanogaster
Author(s) -
Jin Xiaoyi,
Sun Xiaoping,
Song Qisheng
Publication year - 2005
Publication title -
archives of insect biochemistry and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.576
H-Index - 66
eISSN - 1520-6327
pISSN - 0739-4462
DOI - 10.1002/arch.20088
Subject(s) - biology , mutant , drosophila melanogaster , tubulin , ecdysone , gene , microbiology and biotechnology , mutation , genetics , microtubule
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 α‐tubulin in the woc rgl mutant. Our results demonstrated that the mutation in the woc gene caused 20E‐dependent α‐tubulin detyrosination, but had no significant effect on the expression of total α‐ and β‐tubulin in the homozygous woc rgl mutant larvae. Immunocytochemical study revealed that 20E‐induced α‐tubulin detyrosination led to the diminishing of tyrosinated α‐tubulin signals from microtubules, resulting in the disruption of microtubule structure. The composite data suggest that the woc gene may regulate 20E‐dependent α‐tubulin detyrosination and that microtubules may be involved in sterol transport and sterol utilization in insect. Arch. Insect Biochem. Physiol. 60:116–129, 2005. © 2005 Wiley‐Liss, Inc.