【7/12更新】2022年4月1日からのCiNii ArticlesのCiNii Researchへの統合について

Rab35 regulates Arf6 activity through centaurin β2/ACAP2 during neurite outgrowth

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<jats:p>Two small GTPases, Rab and Arf, are well-known molecular switches that function in diverse membrane trafficking routes in a coordinated manner; however, very little is known about the direct cross-talk between Rab and Arf. Although Rab35 and Arf6 were independently reported to regulate same cellular events, including endocytic recycling, phagocytosis, cytokinesis, and neurite outgrowth, the molecular basis that links them remains largely unknown. Here we show evidence that centaurin β2 (also called ACAP2) functions both as a Rab35 effector and as an Arf6-GTPase-activating protein (GAP) during neurite outgrowth of PC12 cells. We found that Rab35 accumulates at Arf6-positive endosomes in response to nerve growth factor (NGF) stimulation and that centaurin β2 is recruited to the same compartment in a Rab35-dependent manner. We further showed by knockdown-rescue experiments that after the Rab35-dependent recruitment of centaurin β2 the Arf6-GAP activity of centaurin β2 at the Arf6-positive endosomes was indispensable for NGF-induced neurite outgrowth. These findings suggest a novel mode of cross-talk between Rab and Arf, i.e., a Rab effector-ArfGAP coupling mechanism, in which ArfGAP is recruited to a specific membrane compartment by its Rab effector function.</jats:p>

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