p120连环蛋白通过Rho家族小G蛋白和钙黏着蛋白调节树突棘和突触的发育。
p120 catenin regulates dendritic spine and synapse development through Rho-family GTPases and cadherins.
作者信息
Elia Lisa P, Yamamoto Miya, Zang Keling, Reichardt Louis F
机构信息
Howard Hughes Medical Institute and Department of Physiology, 1550 Fourth Street, University of California, San Francisco, San Francisco, California 94143, USA.
出版信息
Neuron. 2006 Jul 6;51(1):43-56. doi: 10.1016/j.neuron.2006.05.018.
Abstract
Both the cadherin-catenin complex and Rho-family GTPases have been shown to regulate dendrite development. We show here a role for p120 catenin (p120ctn) in regulating spine and synapse formation in the developing mouse brain. p120catenin gene deletion in hippocampal pyramidal neurons in vivo resulted in reduced spine and synapse densities along dendrites. In addition, p120 catenin loss resulted in reduced cadherin levels and misregulation of Rho-family GTPases, with decreased Rac1 and increased RhoA activity. Analyses in vitro indicate that the reduced spine density reflects aberrant Rho-family GTPase signaling, whereas the effects on spine maturation appear to result from reduced cadherin levels and possibly aberrant Rho-family GTPase signaling. Thus, p120ctn acts as a signal coordinator between cadherins and Rho-family GTPases to regulate cytoskeletal changes required during spine and synapse development.
摘要
钙黏蛋白-连环蛋白复合体和Rho家族小G蛋白都已被证明可调节树突发育。我们在此展示了p120连环蛋白（p120ctn）在调节发育中小鼠大脑的棘突和突触形成中的作用。体内海马锥体神经元中p120连环蛋白基因缺失导致沿树突的棘突和突触密度降低。此外，p120连环蛋白缺失导致钙黏蛋白水平降低以及Rho家族小G蛋白调节异常，Rac1活性降低而RhoA活性增加。体外分析表明，棘突密度降低反映了Rho家族小G蛋白信号异常，而对棘突成熟的影响似乎是由于钙黏蛋白水平降低以及可能的Rho家族小G蛋白信号异常所致。因此，p120ctn作为钙黏蛋白和Rho家族小G蛋白之间的信号协调器，以调节棘突和突触发育过程中所需的细胞骨架变化。
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