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- W2082008165 abstract "During axonal growth, repulsive guidance cues cause growth cone collapse and retraction. In the chick embryo, membranes from the posterior part of the optic tectum containing ephrins are original collapsing factors for axons growing from the temporal retina. We investigated signal transduction pathways in retinal axons underlying this membrane-evoked collapse. Perturbation experiments using pertussis toxin (PTX) showed that membrane-induced collapse is mediated via Go/i proteins, as is the case for semaphorin/collapsin-1–induced collapse. Studies with Indo-1 revealed that growth cone collapse by direct activation of Go/i proteins with mastoparan did not cause elevation of the intracellular Ca2+ level, and thus this signal transduction pathway is Ca2+ independent. Application of the protein phosphatase inhibitor okadaic acid alone induced growth cone collapse in retinal culture, suggesting signals involving protein dephosphorylation. In addition, pretreatment of retinal axons with olomoucine, a specific inhibitor of cdk5 (tau kinase II), prevented mastoparan-evoked collapse. Olomoucine also blocks caudal tectal membrane-mediated collapse. These results suggest that rearrangement of the cytoskeleton is mediated by tau phosphorylation. Immunostaining visualized complementary distributions of tau phospho- and dephosphoisoforms within the growth cone, which also supports the involvement of tau. Taking these findings together, we conclude that cdk5 and tau phosphorylation probably lie downstream of growth cone collapse signaling mediated by PTX-sensitive G proteins. © 1999 John Wiley & Sons, Inc. J Neurobiol 41: 326–339, 1999" @default.
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- W2082008165 date "1999-11-15" @default.
- W2082008165 modified "2023-09-25" @default.
- W2082008165 title "Role of Cdk5 and Tau phosphorylation in heterotrimeric G protein-mediated retinal growth cone collapse" @default.
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- W2082008165 doi "https://doi.org/10.1002/(sici)1097-4695(19991115)41:3<326::aid-neu2>3.0.co;2-w" @default.
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