The mutation without children(rgl) causes ecdysteroid deficiency in third-instar larvae of Drosophila melanogaster

Citation
J. Wismar et al., The mutation without children(rgl) causes ecdysteroid deficiency in third-instar larvae of Drosophila melanogaster, DEVELOP BIO, 226(1), 2000, pp. 1-17
Citations number
68
Categorie Soggetti
Cell & Developmental Biology
Journal title
DEVELOPMENTAL BIOLOGY
ISSN journal
00121606 → ACNP
Volume
226
Issue
1
Year of publication
2000
Pages
1 - 17
Database
ISI
SICI code
0012-1606(20001001)226:1<1:TMWCCE>2.0.ZU;2-4
Abstract
Larvae homozygous for the recessive lethal allele without children(rgl) (wo c(rgl)) fail to pupariate. Application of exogenous 20-hydroxyecdysone elic its puparium formation and pupation. Ecdysteroid titer measurements on muta nt larvae show an endocrine deficiency in the brain-ring gland complex, whi ch normally synthesizes ecdysone, resulting in a failure of the larvae to a chieve a threshold whole body hormone titer necessary for molting. Ultrastr uctural investigation revealed extensive degeneration of the prothoracic ce lls of the ring gland in older larvae. The woe gene, located in polytene ch romosomal region 97F, consists of 11 exons. A 6.8-kb transcript is expresse d throughout development but is absent in the mutant woc(rgl) larvae. The w oe gene encodes a protein of 187 kDa. Eight zinc fingers of the C2-C2 type point to a possible function as a transcription factor. The woc protein sho ws considerable homology to human proteins which have been implicated in bo th mental retardation and a leukemia/lymphoma syndrome. (C) 2000 Academic P ress.