P-element mutations affecting embryonic peripheral nervous system development in Drosophila melanogaster

• Published in: Genetics (Austin) Vol. 139; no. 4; pp. 1663 - 1678
• Main Authors: Kania, A, Salzberg, A, Bhat, M, D'Evelyn, D, He, Y, Kiss, I, Bellen, H.J
• Format: Journal Article
• Language: English
• Published: United States Genetics Soc America 01-04-1995; Genetics Society of America
• Subjects: Animals; cell biology; Chromosome Mapping; cytological mapping; DNA Transposable Elements; Drosophila melanogaster; Drosophila melanogaster - embryology; Drosophila melanogaster - genetics; embryo (animal); embryogenesis; gain of neurons; genetic complementation; Genetics; Insects; insertional mutagenesis; insertions; Investigations; loss of neurons; mutants; Mutation; Nervous system; Neurons; peripheral nerves; Peripheral Nervous System - embryology; Phenotype; transposons
• ISSN: 0016-6731; 1943-2631; 1943-2631
• DOI: 10.1093/genetics/139.4.1663

The Drosophila embryonic peripheral nervous system (PNS) is an excellent model system to study the molecular mechanisms governing neural development. To identify genes controlling PNS development, we screened 2000 lethal P-element insertion strains. The PNS of mutant embryos was examined using the neural specific marker MAb 22C10, and 92 mutant strains were retained for further analysis. Genetic and cytological analysis of these strains shows that 42 mutations affect previously isolated genes that are known to be required for PNS development: longitudinals lacking (19), mastermind (15), numb (4), big brain (2), and spitz (2). The remaining 50 mutations were classified into 29 complementation groups and the P-element insertions were cytologically mapped. The mutants were classified in five major classes on the basis of their phenotype: gain of neurons, loss of neurons, organizational defects, pathfinding defects and morphological defects. Herein we report the preliminary phenotypic characterization of each of these complementation groups as well as the embryonic lacZ expression pattern of each P-element strain. Our analysis indicates that in most of the P-element insertion strains, the lacZ reporter gene is not expressed in the developing PNS.