期刊
JOURNAL OF NEUROSCIENCE
卷 31, 期 3, 页码 1038-1047出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1205-10.2011
关键词
-
资金
- National Science Foundation (NSF) [IBN-0919747, IBN-0548543]
- March of Dimes Foundation [1-FY04-107, 1-FY08-464]
- American Heart Association
- National Institutes of Health [R01 GM083889, 5 T32 MH019957-10, T32 GM00839]
- University and Louis Bevier Graduate and Dissertation Fellowship
- Integrative Graduate Education and Research Traineeship Program on Integratively Engineered Biointerfaces at Rutgers (NSF) [DGE-0333196]
- Pharmaceutical Manufacturers of America Foundation
- Direct For Biological Sciences
- Division Of Integrative Organismal Systems [0919747] Funding Source: National Science Foundation
Little is known about how the neuronal cytoskeleton is regulated when a dendrite decides whether to branch or not. Previously, we reported that postsynaptic density protein 95 (PSD-95) acts as a stop signal for dendrite branching. It is yet to be elucidated how PSD-95 affects the cytoskeleton and how this regulation relates to the dendritic arbor. Here, we show that the SH3 (src homology 3) domain of PSD-95 interacts with a proline-rich region within the microtubule end-binding protein EB3. Overexpression of PSD-95 or mutant EB3 results in a decreased lifetime of EB3 comets in dendrites. In line with these data, transfected rat neurons show that overexpression of PSD-95 results in less organized microtubules at dendritic branch points and decreased dendritogensis. The interaction between PSD-95 and EB3 elucidates a function for a novel region of EB3 and provides a new and important mechanism for the regulation of microtubules in determining dendritic morphology.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据