DEVELOPMENTAL REQUIREMENTS FOR THE ECDYSONELESS (ECD) LOCUS IN DROSOPHILA-MELANOGASTER

Citation
Vc. Henrich et al., DEVELOPMENTAL REQUIREMENTS FOR THE ECDYSONELESS (ECD) LOCUS IN DROSOPHILA-MELANOGASTER, Developmental genetics, 14(5), 1993, pp. 369-377
Citations number
32
Categorie Soggetti
Genetics & Heredity","Developmental Biology
Journal title
ISSN journal
0192253X
Volume
14
Issue
5
Year of publication
1993
Pages
369 - 377
Database
ISI
SICI code
0192-253X(1993)14:5<369:DRFTE(>2.0.ZU;2-W
Abstract
The ecdysoneless locus in Drosophila melonogaster has been defined pre viously by a single conditional mutation, 1(3)ecd1, that causes an ecd ysteroid deficit and larval death at the restrictive temperature, 29-d egrees-C, although the primary role of the mutation in developmental p rocesses has been unclear. Gene dosage and complementation studies rep orted here for ecd1 and five nonconditional lethal alleles indicate th at the ecd locus plays prezygotic and postzygotic roles essential for normal embryonic development, the successful completion of each larval molt, adult eclosion, and female fertility. The ecd locus is also req uired for normal macrochaete differentiation. For each observed phenot ype, the severity of mutational effects was correlated with ecd mutant genotypes. In all cases, ecd1 homozygotes were least affected. Mutant s heteroallelic for and any one of four nonconditional recessive mutat ions were more severely affected than ecd1 homozygotes, revealing thes e as hypomorphic alleles. For all phenotypic effects, mutants heteroal lelic for ecd1 and a dominant mutation (ecd3D) were most severely affe cted. These individuals died during embryogenesis at 29-degrees-C and developed no macrochaetes on the dorsal thorax when transferred to 29- degrees-C during the white prepupal stage. The ecd3D mutation also cau sed female semisterility in heterozygotes. Ecdysteroid regulation has been implicated previously in all the developmental processes disrupte d by these ecd mutations except for macrochaete differentiation. (C) 1 993 Wiley-Liss, Inc.