图片显示的是线虫离断的神经。左图中神经再生基因dlk-1功能正常，向上生长的轴突分支过多且缺乏生长锥，不能到达主神经（每幅图片中靠近顶部的水平生长部分）。中间图片中再生基因被过度激活，其向上生长时带有一个正常的生长锥，且分支也不太多，最终它将到达顶部的主神经。右图中再生基因被破坏，没有神经轴突的再生，只有顶部和底部的残端。
神经细胞在胚胎期具有再生能力，但成年期后大部分细胞便失去再生能力。研究发现外周神经细胞再生能力要强于大脑和脊髓的中枢神经元，但具体机制还不清楚。
研究人员将目光集中到了运动神经元轴突的再生上，轴突是每个神经细胞的缆索状部分，可以将信号传导到其它神经细胞或肌肉。
美国犹他大学的研究小组通过线虫实验发现，线虫dlk-1基因在神经再生调控时起到重要作用。当dlk-1基因大量表达时，研究人员发现神经再生速度比对照组快，而沉默或敲除dlk-1基因，神经细胞彻底失去再生功能。进一步研究表明dlk-1和其他三个基因一起调控整个神经再生通路表达，此通路属于MAPK信号通路。dlk-1基因所表达的DLK-1蛋白在调控中起到重要作用。(生物谷Bioon.com)
生物谷推荐原始出处：
Science DOI: 10.1126/science.1165527
Axon Regeneration Requires a Conserved MAP Kinase Pathway
Marc Hammarlund 1, Paola Nix 2, Linda Hauth 2, Erik M. Jorgensen 3, Michael Bastiani 2*
1 Department of Biology, University of Utah, 257 South 1400 East, Salt Lake City, UT 84112-0840, USA.; Howard Hughes Medical Institute, University of Utah, 257 South 1400 East, Salt Lake City, UT 84112-0840, USA.; Present address: Department of Genetics and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06510, USA.
2 Department of Biology, University of Utah, 257 South 1400 East, Salt Lake City, UT 84112-0840, USA.
3 Department of Biology, University of Utah, 257 South 1400 East, Salt Lake City, UT 84112-0840, USA.; Howard Hughes Medical Institute, University of Utah, 257 South 1400 East, Salt Lake City, UT 84112-0840, USA.
Regeneration of injured neurons can restore function, but most neurons regenerate poorly or not at all. The failure to regenerate, in some cases, is due to a lack of activation of cell-intrinsic regeneration pathways. Thus, these pathways might be targeted for the development of therapies that can restore neuron function after injury or disease. Here, we show that the DLK-1 mitogen-activated protein (MAP) kinase pathway is essential for regeneration in Caenorhabditis elegans motor neurons. Loss of this pathway eliminates regeneration, whereas activating it improves regeneration. Further, these proteins also regulate the later step of growth cone migration. We conclude that after axon injury, activation of this MAP kinase cascade is required to switch the mature neuron from an aplastic state to a state capable of growth.
