The stimulation of dendrite growth by Sema3A requires integrin engagement and focal adhesion kinase
The stimulation of dendrite growth by Sema3A requires integrin engagement and focal adhesion kinase
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DOI：
10.1242/jcs.038232
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发表时间：
2009-06-15
影响因子：
4
通讯作者：
Pueschel, Andreas W.
中科院分区：
文献类型：
--
作者：
Schlomann, Uwe;Schwamborn, Jens C.;Pueschel, Andreas W.
轴突和树突生长的速度和方向取决于多种引导信号和生长因子。信号蛋白3A （Sema3A）对轴突具有驱避作用，对树突具有引诱作用。在这里，我们发现整合素参与的需求区分了海马神经元中轴突和树突对Sema3A的反应。Sema3A通过需要局灶黏附激酶（FAK）的途径促进海马树突的延伸。Sema3A对树突生长的刺激和FAK磷酸化依赖于整合素的参与。与它们在轴突生长锥体坍塌过程中作为Sema3A靶标的功能不同，整合素促进刺激树突延伸。编码β 1整合素或FAK的基因条件失活会阻断Sema3A的促生长作用，但不会阻断轴突生长锥的塌陷。我们的研究结果表明，不同的通路介导了Sema3A对树突生长和轴突生长锥的刺激。
The rate and direction of axon and dendrite growth depend on multiple guidance signals and growth factors. Semaphorin 3A (Sema3A) acts as a repellent for axons and attractant for dendrites. Here, we show that the requirement for integrin engagement distinguishes the response of axons and dendrites to Sema3A in hippocampal neurons. Sema3A promotes the extension of hippocampal dendrites by a pathway that requires focal adhesion kinase (FAK). The stimulation of dendrite growth and FAK phosphorylation by Sema3A depend on integrin engagement. Unlike their function as a target of Sema3A during the collapse of axonal growth cones, integrins facilitate the stimulation of dendrite extension. Conditional inactivation of the genes encoding beta 1 integrin or FAK blocks the growth-promoting effect of Sema3A but not the collapse of axonal growth cones. Our results demonstrate that different pathways mediate the stimulation of dendrite growth and the collapse of axonal growth cones by Sema3A.