Drosophila abl and genetic redundancy in signal transduction.
Genetic studies on Drosophila Abl and, more recently, on mouse c-Abl and c-Src indicate that the functions of these non-receptor tyrosine kinases may duplicate activities of other molecules within signal transduction pathways. In Drosophila, second-site mutations have been recovered that disrupt the redundant functions so that the Abl tyrosine kinase is essential to the formation of axonal connections in the embryonic central nervous system and for attachment of embryonic muscles to the body wall. Molecular isolation and analysis of the genes identified by these second-site mutations should define the molecular basis for the genetic redundancy.
Hoffmann
F M
FM
McArdle Laboratory for Cancer Research, University of Wisconsin, Madison 53706.
D000483:Alleles; D000818:Animals; D003593:Cytoplasm / Q000201:enzymology; D004331:Drosophila melanogaster / Q000196:embryology / Q000235:genetics* / Q000502:physiology; D004625:Embryo, Nonmammalian / Q000201:enzymology; D047108:Embryonic Development; D005314:Embryonic and Fetal Development; D004790:Enzyme Induction; D005804:Genes, Lethal; D016313:Genes, abl; D008957:Models, Genetic; D009154:Mutation; D011499:Protein Processing, Post-Translational; D011505:Protein-Tyrosine Kinases / Q000235:genetics / Q000502:physiology*; D016315:Proto-Oncogene Proteins c-abl / Q000235:genetics / Q000502:physiology*; D015398:Signal Transduction
D011505:Protein-Tyrosine Kinases; D016315:Proto-Oncogene Proteins c-abl