Dual regulation of neuronal morphogenesis by a delta-catenin-cortactin complex and Rho.
Dual regulation of neuronal morphogenesis by a delta-catenin-cortactin complex and Rho.
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DOI：
10.1083/jcb.200211025
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发表时间：
2003-07-07
影响因子：
7.8
通讯作者：
Kosik, Kenneth S
中科院分区：
文献类型：
--
作者：
Martinez, Maria Cruz;Ochiishi, Tomoyo;Majewski, Michael;Kosik, Kenneth S
δ-Catenin是一种神经元蛋白，含有10个Armadillo基序，与经典钙粘蛋白的质膜片段结合。我们报告，δ-连环蛋白相互作用与corpine在酪氨酸磷酸化依赖的方式。这种相互作用发生在δ-连环蛋白序列的一个区域内，该区域也是神经突延伸效应所必需的。Src家族激酶可以磷酸化δ-连环蛋白并通过其多聚脯氨酸束与δ-连环蛋白结合。在酪氨酸磷酸化减少的条件下，δ-连环蛋白与皮质蛋白结合，细胞延伸无分支的初级突起。相反，增加酪氨酸磷酸化会破坏δ-连环蛋白-皮质蛋白复合物。当RhoA被抑制时，δ-连环蛋白增强Rho抑制对分支的影响。我们的结论是δ-连环蛋白有助于在复杂树突树的构建中在神经突延伸和分支之间建立平衡。
δ-Catenin is a neuronal protein that contains 10 Armadillo motifs and binds to the juxtamembrane segment of classical cadherins. We report that δ-catenin interacts with cortactin in a tyrosine phosphorylation–dependent manner. This interaction occurs within a region of the δ-catenin sequence that is also essential for the neurite elongation effects. Src family kinases can phosphorylate δ-catenin and bind to δ-catenin through its polyproline tract. Under conditions when tyrosine phosphorylation is reduced, δ-catenin binds to cortactin and cells extend unbranched primary processes. Conversely, increasing tyrosine phosphorylation disrupts the δ-catenin–cortactin complex. When RhoA is inhibited, δ-catenin enhances the effects of Rho inhibition on branching. We conclude that δ-catenin contributes to setting a balance between neurite elongation and branching in the elaboration of a complex dendritic tree.