Developmental consequences of awd b3, a cell-autonomous lethal mutation of Drosophila induced by hybrid dysgenesis

Abstract

In order to recover mutations affecting imaginal discs in a way which would allow the relevant genes to be readily cloned, a hybrid dysgenic screen was performed for mutations causing late larval/early pupal lethality. This paper describes that mutagenesis procedure and the phenotypes caused by the mutations that were recovered. Of 81 late larval/pupal lethal mutations that were recovered, 20 cause imaginal disc defects. These 20 mutations define 12 different genes. This paper also includes a description of the developmental defects caused by a mutation in one of those 12 genes which we have named abnormal wing discs (awd); the following paper ( C. Dearolf, N. Tripoulas, J. Biggs, and A. Shearn, 1988, Dev. Biol. 129, 169–178 ) describes the cloning of the awd gene and an analysis of its pattern of transcription. awd b3 homozygotes develop at a normal rate until the end of the second larval instar, when their rate of development is reduced. After an extended third larval instar, they form puparia and die. Mutant wing discs have an abnormal morphology and extensive cell death. These abnormal wing discs, and also the leg and eye-antenna discs which appear to be morphologically normal, differentiate poorly or not at all when injected into metamorphosing larvae. Analysis of genetic mosaics indicates that the awd b3 mutation is expressed in a cell-autonomous manner in wing, leg, and eye-antenna discs. The larval brain and proventriculus in awd b3 homozygous third-instar larvae appear to be vacuolated due to the accumulation of lipid droplets. Mutant ovaries are unable to develop when injected into wild-type larvae, although mutant germ cells are capable of producing normal eggs.