RESUMEN
The genes cubitus interruptus (ci), ribosomal protein S3A (RpS3A), and pangolin (pan) are localized within 73 kb in the cytological region 101F-102A on chromosome IV in Drosophila melanogaster. A region of 13 kb harbours the regulatory regions of both ci and pan, transcribed in opposite directions, and a 1.1-kb gene encoding RpS3A. This dense clustering gives rise to very complicated complementation patterns between different alleles in these loci. We investigated this region genetically and molecularly by use of an enhancer trap line (IA5), where the P-element was found to be inserted into the first intron of pan. Screens for imprecise excisions of the P-element were performed, and complementations between new and old established mutant lines were investigated. We found that when mutated or deleted the RpS3A gene gives rise to a Minute phenotype, and we conclude that M(4)101 encodes the ribosomal protein S3A.
Asunto(s)
Proteínas de Unión al ADN/genética , Proteínas de Drosophila , Drosophila melanogaster/genética , Proteínas de Insectos/genética , Proteínas Represoras , Proteínas Ribosómicas/genética , Factores de Transcripción/genética , Animales , Northern Blotting , Elementos Transponibles de ADN , Drosophila melanogaster/embriología , Femenino , Genes de Insecto , Prueba de Complementación Genética , Masculino , beta-Galactosidasa/genéticaRESUMEN
A central question in the development of many branched tubular organs, including the Drosophila trachea, concerns the mechanisms and molecules that control the number and pattern of new branches arising from preexisting vessels. We report on a branching inhibitor, Fusion-6 (Fus-6) produced by specialized tracheal cells to prevent neighboring cells from branching. In Fus-6 mutants, cells that are normally quiescent acquire the branching fate and form an increased number of sprouts emanating from the primary branches. Fus-6 is identified as the headcase (hdc) gene and is expressed in a subset of the cells that extend fusion sprouts to interconnect the tracheal network. hdc expression is regulated by the transcription factor escargot (esg) because it is not expressed in the fusion cells of esg mutants and is ectopically activated in the trachea in response to esg misexpression. We show that the hdc mRNA encodes two overlapping protein products by an unusual suppression of translational termination mechanism. Translational readthrough is necessary for hdc function because rescue of the tracheal mutant phenotype requires the full-length hdc mRNA. In ectopic expression experiments with full-length and truncated hdc constructs, only the full-length cDNA encoding both proteins could inhibit terminal branching. We propose that hdc acts non-autonomously in an inhibitory signaling mechanism to determine the number of cells that will form unicellular sprouts in the trachea.
