Genetic characterization and cloning of Mothers against dpp, a gene required for decapentaplegic function in Drosophila melanogaster
Article Abstract:
A search for gene mutations that alter the sensitive dpp mutant phenotypes in Drosophila melanogaster results in the cloning and characterization of the Mothers against dpp (Mad) gene that codes for a product required for dpp function. Molecular analysis of the MAD protein reveals that it is a member of a new protein family that is conserved among metazoans. Imaginal disk growth, midgut morphogenesis and embryonic dorsal-ventral patterning are defective in Mad mutant animals. Sequencing of a Mad cDNA reveals the presence of three Mad point mutations that affect the coding information.
Publication Name: Genetics
Subject: Biological sciences
ISSN: 0016-6731
Year: 1995
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Genetic screens to identify elements of the decapentaplegic signaling pathway in Drosophila
Article Abstract:
Two types of genetic screens help identify genes associated with the decapentaplegic (dpp) signaling pathway in Drosophila. One of the screens, which help identify genes essential for the help dpp signaling during embryonic dorsal-ventral patterning, reveals one mutation in tolloid and two novel mutations in screw. The second type of screen reveals that dpp signaling at various developmental stages uses functions encoded by Mother against dpp and Medea. Few components of the dpp signaling pathway are titrated by the screw mutations.
Publication Name: Genetics
Subject: Biological sciences
ISSN: 0016-6731
Year: 1995
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Damage control: the pleiotropy of DNA repair genes in Drosophila melanogaster
Article Abstract:
Studies of DNA repair genes in Drosophila melanogaster elucidate their functions in eukaryotes. Special classes of proteins that can recognize different types of DNA damage have been identified in various organisms. Mei-41 gene mutations in Drosophila melanogaster were first characterized on the basis of a damage in meiotic recombination. Research shows that mutations in mei-41 result in severe chromosome damage and instability in mitotic cells.
Publication Name: Genetics
Subject: Biological sciences
ISSN: 0016-6731
Year: 1998
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