ArticleMechanisms of development
The receptor protein tyrosine phosphatase PTP69D antagonizes Abl tyrosine kinase to guide axons in Drosophila.
Article in Mechanisms of development. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Structure-function analyses of tyrosine phosphatase PTP69D in giant fiber synapse formation of Drosophila.Molecular and cellular neurosciences · 2015Article
- Extracellular matrix and its receptors in Drosophila neural development.Developmental neurobiology · 2011Review
- Noncanonical Notch function in motor axon guidance is mediated by Rac GTPase and the GEF1 domain of Trio.Developmental dynamics : an official publication of the American Association of Anatomists · 2011Article
- ABL tyrosine kinases: evolution of function, regulation, and specificity.Science signaling · 2010Review
- Article
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3 authors.
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Abstract
During Drosophila embryogenesis, both the cytoplasmic Abelson tyrosine kinase (Abl) and the membrane bound tyrosine phosphatase PTP69D are required for proper guidance of CNS and motor axons. We provide evidence that PTP69D modulates signaling by Abl and its antagonist, Ena. An Abl loss-of function mutation dominantly suppresses most Ptp69D mutant phenotypes including larval/pupal lethality and CNS and motor axon defects, while increased Abl and decreased Ena expression dramatically increase the expressivity of Ptp69D axonal defects. In contrast, Ptp69D mutations do not affect Abl mutant phenotypes. These results support the hypothesis that PTP69D antagonizes the Abl/Ena genetic pathway, perhaps as an upstream regulator. We also find that mutation of the gene encoding the cytoplasmic Src64B tyrosine kinase exacerbates Ptp69D phenotypes, suggesting that two different cytoplasmic tyrosine kinases, Abl and Src64B, modify PTP69D-mediated axon patterning in quite different ways.
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