日本和美国科学家组成的一个联合研究小组日前在利用老鼠进行的试验中，成功发现视神经再生机制，同时使老鼠受损的视神经实现了再生。

东京都神经科学综合研究所研究员行方和彦、原田高幸与美国科学家共同发现，一种名为“Dock3”的蛋白质在视神经细胞中发挥着重要作用。向老鼠的视神经细胞中植入能够制造这种蛋白质的基因后，视神经细胞活跃程度就会提高。

接下来，科学家们利用一种转基因老鼠与正常老鼠进行对比试验。转基因老鼠体内制造“Dock3”蛋白质的能力是正常老鼠的5倍左右。当这两种老鼠的视神经受损后，正常老鼠的视神经几乎不会再生，但是转基因老鼠的视神经却在很大程度上恢复了。

科学家由此认为，“Dock3”蛋白质是使视神经细胞活跃，从而促进视神经再生的关键。由于人体内也存在制造同样蛋白质的基因，科学家期待这一研究成果能够帮助开发出新的治疗和预防视神经受损的方法。这一研究成果已经刊登在新一期美国《国家科学院院刊》（PNAS）上。

        参考文献：Published online before print April 5, 2010, doi: 10.1073/pnas.0914514107
PNAS April 20, 2010 vol. 107 no. 16 7586-7591

Dock3 induces axonal outgrowth by stimulating membrane recruitment of the WAVE complex

Atypical Rho-guanine nucleotide exchange factors (Rho-GEFs) that contain Dock homology regions (DHR-1 and DHR-2) are expressed in a variety of tissues; however, their functions and mechanisms of action remain unclear. We identify key conserved amino acids in the DHR-2 domain that are critical for the catalytic activity of Dock-GEFs (Dock1–4). We further demonstrate that Dock-GEFs directly associate with WASP family verprolin-homologous (WAVE) proteins through the DHR-1 domain. Brain-derived neurotrophic factor (BDNF)-TrkB signaling recruits the Dock3/WAVE1 complex to the plasma membrane, whereupon Dock3 activates Rac and dissociates from the WAVE complex in a phosphorylation-dependent manner. BDNF induces axonal sprouting through Dock-dependent Rac activation, and adult transgenic mice overexpressing Dock3 exhibit enhanced optic nerve regeneration after injury without affecting WAVE expression levels. Our results highlight a unique mechanism through which Dock-GEFs achieve spatial and temporal restriction of WAVE signaling, and identify Dock-GEF activity as a potential therapeutic target for axonal regeneration.