The gang of four gene regulates growth and patterning of the developing Drosophila eye

• Published in: Fly (Austin, Tex.) Tex.), 2010-04, Vol.4 (2), p.104-116
• Main Authors: Beam, Carolyn K., Moberg, Kenneth H.
• Format: Article
• Language: English
• Subjects: Alleles; Animals; Animals, Genetically Modified; Base Sequence; Binding; Biology; Bioscience; Body Patterning - genetics; Calcium; Cancer; Cell; Cell Death - genetics; Chromosome Mapping; Cycle; DNA Primers - genetics; Drosophila melanogaster - genetics; Drosophila melanogaster - growth & development; Drosophila melanogaster - metabolism; Drosophila Proteins - genetics; Drosophila Proteins - metabolism; Eye - growth & development; Eye - metabolism; Female; Gene Expression Regulation, Developmental; Genes, Insect; Genetic Complementation Test; Green Fluorescent Proteins - genetics; Green Fluorescent Proteins - metabolism; Landes; Male; MAP Kinase Signaling System - genetics; Models, Biological; Mutation; Organogenesis; Phenotype; Phosphoprotein Phosphatases - genetics; Phosphoprotein Phosphatases - metabolism; Proteins; Receptors, Notch - genetics; Receptors, Notch - metabolism; Wings, Animal - growth & development; Wings, Animal - metabolism
• ISSN: 1933-6934; 1933-6942
• DOI: 10.4161/fly.4.2.11890

We report here the identification of a novel complementation group in the fruit fly Drosophila melanogaster named gang of four (gfr). Mutations in gfr disrupt patterns of cell differentiation in the eye and increase eye size through a proliferative mechanism that can be enhanced by a block in apoptosis. gfr mutant cells show several features of deregulated Ras/MAP kinase activity, including reduced expression of the Capicua growth suppressing transcription factor and synthetically lethality with alleles of the Jun N-terminal kinase phosphatase puckered. gfr alleles also upreguate Notch activity in the eye. Thus, gfr alleles appear to elicit growth and patterning phenotypes via effects on multiple signaling pathways. Moreover, the gfr alleles behave as gain-of-function lesions and overexpress the gene bruno-3 (bru-3), which is located at the genomic region to which gfr lesions map. Genetic reduction of bru-3 suppresses phenotypes caused by gfr alleles, and like gfr alleles, overexpression of bru-3 depresses levels of Cic protein, indicating that overexpression of bru-3 is central to gfr mutant phenotypes.