Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel.
Neuroplasticity Group, Leibniz Institute for Neurobiology, Brenneckestraße 6, Magdeburg 39118, Germany.
Trends Neurosci. 2015 Feb;38(2):108-16. doi: 10.1016/j.tins.2014.12.001. Epub 2014 Dec 19.
Local signaling events at synapses or axon terminals must be communicated to the nucleus to elicit transcriptional responses. The lengths of neuronal processes pose a significant challenge for such intracellular communication. This challenge is met by mechanisms ranging from rapid signals encoded in calcium waves to slower macromolecular signaling complexes carried by molecular motors. Here we summarize recent findings on macromolecular signaling from the synapse to the nucleus, in comparison to those employed in injury signaling along axons. A number of common themes emerge, including combinatorial signal encoding by post-translational mechanisms such as differential phosphorylation and proteolysis, and conserved roles for importins in coordinating signaling complexes. Neurons may integrate ionic flux with motor-transported signals as a temporal code for synaptic plasticity signaling.
在突触或轴突末端的局部信号事件必须传递到细胞核，以引发转录反应。神经元过程的长度对这种细胞内通讯构成了重大挑战。这种挑战通过从钙波中编码的快速信号到由分子马达携带的较慢的大分子信号复合物的机制来解决。在这里，我们总结了最近关于从突触到细胞核的大分子信号的发现，与那些在沿着轴突的损伤信号中使用的发现进行了比较。出现了一些共同的主题，包括通过翻译后机制（如差异磷酸化和蛋白水解）进行组合信号编码，以及导入蛋白在协调信号复合物方面的保守作用。神经元可以将离子通量与马达运输的信号整合为突触可塑性信号的时间代码。
