In particular, the potential role of the large family of transient receptor potential (TRP) channels in dendrite morphogenesis However, the role of other calcium channels in the regulation of dendrite development remains largely to be elucidated. Voltage-sensitive calcium channels (VSCCs) and NMDA receptors provide a major mode of calcium entry in neurons and triggerĭownstream signaling cascades that control dendrite development ( Konur and Ghosh 2005 Cline and Haas 2008). Interest because disturbances in dendrite structure are featured in diverse neurological diseases, including mental retardationĪnd autism spectrum disorders ( Kaufmann and Moser 2000 Dierssen and Ramakers 2006 Pardo and Eberhart 2007).Ĭalcium signaling plays a central role in the regulation of dendrite morphogenesis and connectivity in the developing brain Beyond providing a better understanding of brain development, studies of dendrite morphogenesis have garnered increasing 2000 Jan and Jan 2003 Grueber and Jan 2004 de la Torre-Ubieta and Bonni 2011). ![]() The regulation of dendrite development is essential for the establishment of neuronal circuits in the brain ( Hausser et al. To a ubiquitin ligase pathway at the centrosome and thereby orchestrates dendrite patterning and connectivity in the brain. Our findings define a novel function for TRPC5 that couples calcium signaling Regulate dendrite morphogenesis in neurons. Accordingly, centrosomal CaMKIIβ signaling mediates the ability of TRPC5 to Ubiquitin ligase Cdc20-APC at the centrosome. With CaMKIIβ, but not the closely related kinase CaMKIIα, and thereby induces the CaMKIIβ-dependent phosphorylation of the Remarkably, TRPC5 forms a complex specifically Kinase II β (CaMKIIβ) as a critical effector of TRPC5 function in neurons. We identify the major protein kinase calcium/calmodulin-dependent Molecular basis of TRPC5's function in dendrite patterning. Correlating with impaired dendrite patterning in the cerebellar cortex,īehavioral analyses reveal that TRPC5 knockout mice have deficits in gait and motor coordination. The cerebellar cortex in a cell-autonomous manner. ![]() In vivo RNAi analyses suggest that TRPC5 regulates dendrite morphogenesis in Strikingly, TRPC5 knockout mice harbor long, highly branched granule neuron dendrites with impaired dendriticĬlaw differentiation in the cerebellar cortex. Here, we identifyĪn essential function for TRPC5, a member of the canonical TRP subfamily, in the regulation of dendrite patterning in the However,ĭevelopmental roles for TRP channels in the establishment of neuronal connectivity remain largely unexplored. Transient receptor potential (TRP) channels have been implicated as sensors of diverse stimuli in mature neurons.
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