Identification of chromosomal regions involved in decapentaplegic function in drosophila

• Published in: Genetics (Austin) Vol. 149; no. 1; pp. 203 - 215
• Main Authors: Nicholls, R.E, Gelbart, W.M
• Format: Journal Article
• Language: English
• Published: United States Genetics Soc America 01-05-1998; Genetics Society of America
• Subjects: AILE; ALAS; ALLELES; ANIMAL CUTICLE; Animals; Bacterial Proteins - genetics; BLOOD VEINS; CELL DIFFERENTIATION; CHROMOSOMAL DEFICIENCIES; Chromosome Mapping; CUTICULA ANIMAL; CUTICULE ANIMALE; DIFERENCIACION CELULAR; DIFFERENCIATION CELLULAIRE; DNA-Binding Proteins - genetics; DPP LOCUS; DROSOPHILA MELANOGASTER; Drosophila Proteins; FACTEUR DE CROISSANCE TRANSFORMANT; FACTOR DE CRECIMIENTO TRANSFORMANTE; FENOTIPOS; GENE; GENE INTERACTION; GENE RECESSIF; GENES; GENES RECESIVOS; Genetics; INDUCED MUTATION; Insect Proteins - genetics; Insect Proteins - physiology; Insects; INTERACCION DE GENES; INTERACTION GENIQUE; LARVAE; LARVAS; LARVE; LOCI; LOCUS; Molecular biology; MUTACION INDUCIDA; MUTATION PROVOQUEE; PHENOTYPE; PHENOTYPES; RECESSIVE GENES; RECESSIVE LETHALS; SEGREGACION; SEGREGATION; Sequence Deletion; Tolloid-Like Metalloproteinases; Trans-Activators; Transcription Factors; TRANSFORMING GROWTH FACTOR; Transforming Growth Factor beta - genetics; VEINE; VENAS; WINGS
• DOI: 10.1093/genetics/149.1.203
• EISSN: 1943-2631
• ISSN: 0016-6731; 1943-2631

Signaling molecules of the transforming growth factor beta (TGF-beta) family contribute to numerous developmental processes in a variety of organisms. However, our understanding of the mechanisms which regulate the activity of and mediate the response to TGF-beta family members remains incomplete. The product of the Drosophila decapentaplegic (dpp) locus is a well-characterized member of this family. We have taken a genetic approach to identify factors required for TGF-beta function in Drosophila by testing for genetic interactions between mutant alleles of dpp and a collection of chromosomal deficiencies. Our survey identified two deficiencies that act as maternal enhancers of recessive embryonic lethal alleles of dpp. The enhanced individuals die with weakly ventralized phenotypes. These phenotypes are consistent with a mechanism whereby the deficiencies deplete two maternally provided factors required for dpp's role in embryonic dorsal-ventral pattern formation. One of these deficiencies also appears to delete a factor required for dpp function in wing vein formation. These deficiencies remove material from the 54F-55A and 66B-66C polytene chromosomal regions, respectively. As neither of these regions has been previously implicated in dpp function, we propose that each of the deficiencies removes a novel factor or factors required for dpp function.