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C R Dearolf

Publications and source records attributed to C R Dearolf.

20 records · Page 2Linked to original sources
PubMed1988

Developmental consequences of awdb3, a cell-autonomous lethal mutation of Drosophila induced by hybrid dysgenesis.

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. awdb3 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 awdb3 mutation is expressed in a cell-autonomous manner in wing, leg, and eye-antenna discs. The larval brain and proventriculus in awdb3 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.

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PubMed1988

Molecular consequences of awdb3, a cell-autonomous lethal mutation of Drosophila induced by hybrid dysgenesis.

The abnormal wing disc locus, which is at salivary gland chromosome position 100C-D of the Drosophila melanogaster genome, has been identified by a recessive lethal mutation, awdb3, induced by hybrid dysgenesis. When homozygous, this mutation causes abnormal development of the brain, the ovaries, and the larger imaginal discs as described in the preceding paper (C.R. Dearolf, E. Hersperger, and A. Shearn, 1988, Dev. Biol. 129, 159-168). The DNA corresponding to this locus was isolated from a genomic library prepared from awdb3 heterozygotes by screening with a P-element probe. The awdb3 allele resulted from the insertion of a P-element fragment into a gene that encodes an 0.8-kb poly(A)+ RNA. In mutant larvae, that 0.8-kb transcript is replaced by two chimeric transcripts that are 0.7 and 1.3 kb in length, both of which contain P-element and awd sequences. The wild-type awd+ gene transcript is most abundant during the second and third larval instars but is found at a lower level during every developmental stage as well as in continuous cell lines. Thus the awd+ gene transcript can be detected in normal larvae at a developmental stage long before defects are expressed in mutant larvae. Moreover, some tissues, for example the salivary gland of nonmutant, third-instar larvae, contain high levels of this transcript, even though these tissues appear to develop normally in mutant larvae.

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