圖片顯示的是線蟲離斷的神經(jīng),。左圖中神經(jīng)再生基因dlk-1功能正常，向上生長的軸突分支過多且缺乏生長錐,，不能到達主神經(jīng)（每幅圖片中靠近頂部的水平生長部分）,。中間圖片中再生基因被過度激活，其向上生長時帶有一個正常的生長錐,，且分支也不太多,，最終它將到達頂部的主神經(jīng)。右圖中再生基因被破壞,，沒有神經(jīng)軸突的再生,，只有頂部和底部的殘端。
神經(jīng)細胞在胚胎期具有再生能力,，但成年期后大部分細胞便失去再生能力,。研究發(fā)現(xiàn)外周神經(jīng)細胞再生能力要強于大腦和脊髓的中樞神經(jīng)元，但具體機制還不清楚,。
研究人員將目光集中到了運動神經(jīng)元軸突的再生上,，軸突是每個神經(jīng)細胞的纜索狀部分，可以將信號傳導到其它神經(jīng)細胞或肌肉,。
美國猶他大學的研究小組通過線蟲實驗發(fā)現(xiàn),，線蟲dlk-1基因在神經(jīng)再生調控時起到重要作用。當dlk-1基因大量表達時,，研究人員發(fā)現(xiàn)神經(jīng)再生速度比對照組快,，而沉默或敲除dlk-1基因，神經(jīng)細胞徹底失去再生功能,。進一步研究表明dlk-1和其他三個基因一起調控整個神經(jīng)再生通路表達,，此通路屬于MAPK信號通路。dlk-1基因所表達的DLK-1蛋白在調控中起到重要作用,。(生物谷Bioon.com)
生物谷推薦原始出處：
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.
