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GENETIC-CHARACTERIZATION AND CLONING OF MOTHERS AGAINST DPP, A GENE REQUIRED FOR DECAPENTAPLEGIC FUNCTION IN DROSOPHILA-MELANOGASTER
Author(s): SEKELSKY JJ, NEWFELD SJ, RAFTERY LA, CHARTOFF EH, GELBART WM
Source: GENETICS    Volume: 139    Issue: 3    Pages: 1347-1358    Published: MAR 1995  
Times Cited: 394     References: 59     
Abstract: The decapentaplegic (dpp) gene of Drosophila melanogaster encodes a growth factor that belongs to the transforming growth factor-beta (TGF-beta) superfamily and that plays a central role in multiple cell-cell signaling events throughout development. Through genetic screens we are seeking to identify other functions that act upstream, dowstream or in concert with dpp to mediate its signaling role. We report here the genetic characterization and cloning of Mothers against dpp (Mad), a gene identified in two such screens. Mad loss-of-function mutations interact with dpp alleles to enhance embryonic dorsal-ventral patterning defects, as well as adult appendage defects, suggesting a role for Mad in mediating some aspect of dpp function. In support of this, homozygous Mad mutant animals exhibit defects in midgut morphogenesis, imaginal disk development and embryonic dorsal-ventral patterning that are very reminiscent of dpp mutant phenotypes. We cloned the Mad region and identified the Mad transcription unit through germline transformation rescue. We sequenced a Mad cDNA and identified three Mad point mutations that alter the coding information. The predicted MAD polypeptide lacks known protein motifs, but has strong sequence similarity to three polypeptides predicted from genomic sequence from the nematode Caenorhabditis elegans. Hence, MAD is a member of a novel, highly conserved protein family.
Document Type: Article
Language: English
Addresses:
1. HARVARD UNIV, BIOL LABS, CAMBRIDGE, MA 02138 USA
Publisher: GENETICS, 428 EAST PRESTON ST, BALTIMORE, MD 21202
Subject Category: Genetics & Heredity
IDS Number: QJ968
ISSN: 0016-6731
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