期刊
JOURNAL OF NEUROSCIENCE
卷 28, 期 28, 页码 7047-7056出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0451-08.2008
关键词
dendrite; delta-catenin; erbin; LAP proteins; localization; PDZ
资金
- Howard Hughes Medical Institute Funding Source: Medline
- NINDS NIH HHS [P01 NS016033, P01 NS016033-26] Funding Source: Medline
The LAP [leucine-rich and postsynaptic density-95/Discs large/zona occludens-1 (PDZ)] protein erbin and delta-catenin, a component of the cadherin-catenin cell adhesion complex, are highly expressed in neurons and associate through PDZ-mediated interaction, but have incompletely characterized neuronal functions. We show that short hairpin RNA-mediated knockdown of erbin and knockdown or genetic ablation of delta-catenin severely impaired dendritic morphogenesis in hippocampal neurons. Simultaneous loss of erbin and delta-catenin does not enhance severity of this phenotype. The dendritic phenotype observed after erbin depletion is rescued by overexpression of delta-catenin and requires a domain in delta-catenin that has been shown to regulate dendritic branching. Knockdown of delta-catenin cannot be rescued by overexpression of erbin, indicating that erbin is upstream of delta-catenin. delta-Catenin-null neurons have no alterations in global levels of active Rac1/RhoA. Knockdown of erbin results in alterations in localization of delta-catenin. These results suggest a critical role for erbin in regulating dendritic morphogenesis by maintaining appropriate localization of delta-catenin.
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