Drosophila C-Terminal Src Kinase Negatively Regulates Organ Growth and Cell Proliferation through Inhibition of the Src, Jun N-Terminal Kinase, and STAT Pathways
Copyright policy )Drosophila C-Terminal Src Kinase Negatively Regulates Organ Growth and Cell Proliferation through Inhibition of the Src, Jun N-Terminal Kinase, and STAT Pathways
Src family kinases regulate multiple cellular processes including proliferation and oncogenesis. C-terminal Src kinase (Csk) encodes a critical negative regulator of Src family kinases. We demonstrate that the Drosophila melanogaster Csk ortholog, dCsk, functions as a tumor suppressor: dCsk mutants display organ overgrowth and excess cellular proliferation. Genetic analysis indicates that the dCsk(-/-) overgrowth phenotype results from activation of Src, Jun kinase, and STAT signal transduction pathways. In particular, blockade of STAT function in dCsk mutants severely reduced Src-dependent overgrowth and activated apoptosis of mutant tissue. Our data provide in vivo evidence that Src activity requires JNK and STAT function.
- New York University United States
- Washington University in St. Louis United States
- University of Mary United States
- Washington University in St. Louis School of Medicine United States
- Washington University in St. Louis United States
Expressed Sequence Tags, Genotype, Models, Genetic, Cell Cycle, JNK Mitogen-Activated Protein Kinases, Protein-Tyrosine Kinases, Flow Cytometry, Immunohistochemistry, Models, Biological, CSK Tyrosine-Protein Kinase, DNA-Binding Proteins, Phenotype, Larva, Mutation, Microscopy, Electron, Scanning, Animals, Drosophila Proteins, Drosophila, Mitogen-Activated Protein Kinases, Cell Division
Expressed Sequence Tags, Genotype, Models, Genetic, Cell Cycle, JNK Mitogen-Activated Protein Kinases, Protein-Tyrosine Kinases, Flow Cytometry, Immunohistochemistry, Models, Biological, CSK Tyrosine-Protein Kinase, DNA-Binding Proteins, Phenotype, Larva, Mutation, Microscopy, Electron, Scanning, Animals, Drosophila Proteins, Drosophila, Mitogen-Activated Protein Kinases, Cell Division
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