Fak56 functions downstream of integrin alphaPS3betanu and suppresses MAPK activation in neuromuscular junction growth

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Fak56 functions downstream of integrin alphaPS3betanu and suppresses MAPK activation in neuromuscular junction growth

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dc.contributor.author Tsai, Pei-I
dc.contributor.author Kao, Hsiu-Hua
dc.contributor.author Grabbe, Caroline
dc.contributor.author Lee, Yu-Tao
dc.contributor.author Ghose, Aurnab
dc.contributor.author Lai, Tzu-Ting
dc.contributor.author Peng, Kuan-Po
dc.contributor.author Palmer, Ruth H
dc.contributor.author Chen, Ruey-Hwa
dc.contributor.author Yeh, Shih-Rung
dc.contributor.author Chien, Cheng-Ting
dc.contributor.author Van Vactor, David L.
dc.date.accessioned 2011-04-26T00:53:26Z
dc.date.issued 2008
dc.identifier.citation Tsai, Pei-I, Hsiu-Hua Kao, Caroline Grabbe, Yu-Tao Lee, Aurnab Ghose, Tzu-Ting Lai, Kuan-Po Peng, et al. 2008. Fak56 functions downstream of integrin alphaPS3betanu and suppresses MAPK activation in neuromuscular junction growth. Neural Development 3: 26. en_US
dc.identifier.issn 1749-8104 en_US
dc.identifier.uri http://nrs.harvard.edu/urn-3:HUL.InstRepos:4875876
dc.description.abstract Background: Focal adhesion kinase (FAK) functions in cell migration and signaling through activation of the mitogen-activated protein kinase (MAPK) signaling cascade. Neuronal function of FAK has been suggested to control axonal branching; however, the underlying mechanism in this process is not clear. Results: We have generated mutants for the Drosophila FAK gene, Fak56. Null Fak56 mutants display overgrowth of larval neuromuscular junctions (NMJs). Localization of phospho-FAK and rescue experiments suggest that Fak56 is required in presynapses to restrict NMJ growth. Genetic analyses imply that FAK mediates the signaling pathway of the integrin αPS3βν heterodimer and functions redundantly with Src. At NMJs, Fak56 downregulates ERK activity, as shown by diphospho-ERK accumulation in Fak56 mutants, and suppression of Fak56 mutant NMJ phenotypes by reducing ERK activity. Conclusion: We conclude that Fak56 is required to restrict NMJ growth during NMJ development. Fak56 mediates an extracellular signal through the integrin receptor. Unlike its conventional role in activating MAPK/ERK, Fak56 suppresses ERK activation in this process. These results suggest that Fak56 mediates a specific neuronal signaling pathway distinct from that in other cellular processes. en_US
dc.language.iso en_US en_US
dc.publisher BioMed Central en_US
dc.relation.isversionof doi:10.1186/1749-8104-3-26 en_US
dc.relation.hasversion http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2576229/pdf/ en_US
dash.license LAA
dc.title Fak56 functions downstream of integrin alphaPS3betanu and suppresses MAPK activation in neuromuscular junction growth en_US
dc.type Journal Article en_US
dc.description.version Version of Record en_US
dc.relation.journal Neural Development en_US
dash.depositing.author Van Vactor, David L.
dc.date.available 2011-04-26T00:53:26Z
dash.affiliation.other HMS^Cell Biology en_US

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