PubMed Health⌕ Search

Biomedical subjects

J R Girton

Publications and source records attributed to J R Girton.

5 recordsLinked to original sources
PubMed1992

The suppressor of forked locus in Drosophila melanogaster: genetic and molecular analyses.

The suppressor of forked, su(f) locus is one of a class of loci in Drosophila whose mutant alleles are trans-acting allele-specific modifiers of transposable element-insertion mutations at other loci. Mutations of su(f) suppress gypsy insert alleles of forked and enhance the copia insert allele white apricot. Our investigations of su(f) include genetic and molecular analyses of 19 alleles to determine the numbers and types of genetic functions present at the locus. Our results suggest the su(f) locus contains multiple genetic functions. There are two distinct modifier functions and two vital functions. One modifier function is specific for enhancement and the other for suppression. One vital function is required for normal ecdysterone production in the third larval instar, the other is not. We present a restriction map of the su(f) genomic region and the results of an RFLP analysis of several su(f) alleles.

Alleles↗
PubMed1992

Blackpatch, a neural degeneration mutation that interacts with the Notch locus in Drosophila.

We have identified a gene in Drosophila melanogaster that is involved in the development of the adult eye and optic lobe of the brain and that interacts with facet alleles at the Notch locus. We have named this locus Blackpatch (Bpt). Mutant alleles of Bpt produce a variety of abnormal phenotypes in the presence of facet alleles. These phenotypes include neural degeneration in the eye and in the optic lobe of the adult brain that begins 60 hr after pupariation and produces a dark, necrotic eye spot in the adult eye. Other phenotypes include recessive embryonic lethality, pharate adult lethality, and premature adult death. We have isolated and characterized 10 Bpt alleles, all of which yield the neural eye/brain degeneration phenotype in individuals who are also homozygous or hemizygous for facet mutations. Only some of the facet alleles interact with Bpt. Bpt mutations also interact with the split mutation but do not interact with other types of Notch mutation. Somatic mosaic analysis and imaginal disc transplantation experiments suggest that the optic lobe of the brain may be the focus of Bpt action. We conclude that the Notch and Bpt genes have important functions during the interaction between the retina and the optic lobe of the brain.

Alleles↗
PubMed1992

A genetic analysis of deltex and its interaction with the Notch locus in Drosophila melanogaster.

During Drosophila development networks of genes control the developmental pathways that specify cell fates. The Notch gene is a well characterized member of some cell fate pathways, and several other genes belonging to these same pathways have been identified because they share a neurogenic null phenotype with Notch. However, it is unlikely that the neurogenic genes represent all of the genes in these pathways. The goal of this research was to use a genetic approach to identify and characterize one of the other genes that acts with Notch to specify cell fate. Mutant alleles of genes in the same pathway should have phenotypes similar to Notch alleles and should show phenotypic interactions with Notch alleles. With this approach we identified the deltex gene as a potential cell fate gene. An extensive phenotypic characterization of loss-of-function deltex phenotypes showed abnormalities (such as thick wing veins, double bristles and extra cone cells) that suggest that deltex is involved in cell fate decision processes. Phenotypic interactions between deltex and Notch as seen in double mutants showed that Notch and deltex do not code for duplicate functions and that the two genes function together in many different developing tissues. The results of these investigations lead to the conclusion that the deltex gene functions with the Notch gene in one or more developmental pathways to specify cell fate.

Animals↗