8月11日,，《神經(jīng)科學(xué)雜志》（The Journal of Neuroscience）發(fā)表了中國科學(xué)院上海生命科學(xué)研究院神經(jīng)科學(xué)研究所的研究成果：“遷移神經(jīng)元中前導(dǎo)突起頂端通過促進(jìn)肌動蛋白纖維向前流動驅(qū)動胞體遷移”。該項(xiàng)工作主要由何珉和張正洪等在袁小兵研究員指導(dǎo)下完成。
神經(jīng)元遷移涉及細(xì)胞體和前導(dǎo)突起頂端的協(xié)同運(yùn)動,，然而細(xì)胞的不同部位，特別是突起頂端和細(xì)胞后方,，在胞體運(yùn)動中分別發(fā)揮怎樣的作用仍然有待闡述,。何珉及其同事通過局部灌流干擾細(xì)胞骨架成分的方法研究了神經(jīng)元遷移的動力原理。他們發(fā)現(xiàn)與不遷移的神經(jīng)元相比,，遷移神經(jīng)元前導(dǎo)突起頂端的生長錐樣結(jié)構(gòu)更加活躍,，切除生長錐或抑制生長錐動態(tài)都會抑制胞體的遷移。局部破壞引導(dǎo)突起中間的肌動蛋白纖維也會阻止胞體的遷移,，而破壞引導(dǎo)突起中間或胞體處的微管會加速胞體的運(yùn)動,。在轉(zhuǎn)入GFP-alpha-actinin 的神經(jīng)元中，利用熒光斑點(diǎn)成像技術(shù)（Fluorescent speckle microscopy, FSM）觀察到伴隨胞體向前運(yùn)動,，前導(dǎo)突起中存在肌動蛋白纖維向前方的流動,。進(jìn)而發(fā)現(xiàn)肌動蛋白纖維的流動對胞體運(yùn)動是必需的，且肌動蛋白纖維的流動有賴于細(xì)胞內(nèi)肌球蛋白前高后低的活性分布,。這項(xiàng)研究表明,，遷移神經(jīng)元中前導(dǎo)突起頂端通過肌球蛋白介導(dǎo)的肌動蛋白纖維流動活躍的拉動胞體向前運(yùn)動。
該工作得到了中國科學(xué)院,、國家科技部,、自然科學(xué)基金委的資助。（生物谷Bioon.com）
生物谷推薦原文出處：
The Journal of Neuroscience doi:10.1523/JNEUROSCI.0240-10.2010
Leading Tip Drives Soma Translocation via Forward F-Actin Flow during Neuronal Migration
Min He,1,2 Zheng-hong Zhang,1 Chen-bing Guan,1 Di Xia,1 and Xiao-bing Yuan1
1Institute of Neuroscience and State Key Laboratory of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China, and 2Graduate School of the Chinese Academy of Sciences, Shanghai 200031, China
Neuronal migration involves coordinated extension of the leading process and translocation of the soma, but the relative contribution of different subcellular regions, including the leading process and cell rear, in driving soma translocation remains unclear. By local manipulation of cytoskeletal components in restricted regions of cultured neurons, we examined the molecular machinery underlying the generation of traction force for soma translocation during neuronal migration. In actively migrating cerebellar granule cells in culture, a growth cone (GC)-like structure at the leading tip exhibits high dynamics, and severing the tip or disrupting its dynamics suppressed soma translocation within minutes. Soma translocation was also suppressed by local disruption of F-actin along the leading process but not at the soma, whereas disrupting microtubules along the leading process or at the soma accelerated soma translocation. Fluorescent speckle microscopy using GFP--actinin showed that a forward F-actin flow along the leading process correlated with and was required for soma translocation, and such F-actin flow depended on myosin II activity. In migrating neurons, myosin II activity was high at the leading tip but low at the soma, and increasing or decreasing this front-to-rear difference accelerated or impeded soma advance. Thus, the tip of the leading process actively pulls the soma forward during neuronal migration through a myosin II-dependent forward F-actin flow along the leading process.
