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(zhǎng)的軸突分支過(guò)多且缺乏生長(zhǎng)錐，不能到達(dá)主神經(jīng)（每幅圖片中靠近頂部的水平生長(zhǎng)部分）,。中間圖片中再生基因被過(guò)度激活,，其向上生長(zhǎng)時(shí)帶有一個(gè)正常的生長(zhǎng)錐，且分支也不太多,，最終它將到達(dá)頂部的主神經(jīng),。右圖中再生基因被破壞，沒(méi)有神經(jīng)軸突的再生,，只有頂部和底部的殘端,。
神經(jīng)細(xì)胞在胚胎期具有再生能力，但成年期后大部分細(xì)胞便失去再生能力,。研究發(fā)現(xiàn)外周神經(jīng)細(xì)胞再生能力要強(qiáng)于大腦和脊髓的中樞神經(jīng)元,，但具體機(jī)制還不清楚。
研究人員將目光集中到了運(yùn)動(dòng)神經(jīng)元軸突的再生上,，軸突是每個(gè)神經(jīng)細(xì)胞的纜索狀部分,，可以將信號(hào)傳導(dǎo)到其它神經(jīng)細(xì)胞或肌肉。
美國(guó)猶他大學(xué)的研究小組通過(guò)線蟲實(shí)驗(yàn)發(fā)現(xiàn),，線蟲dlk-1基因在神經(jīng)再生調(diào)控時(shí)起到重要作用,。當(dāng)dlk-1基因大量表達(dá)時(shí)，研究人員發(fā)現(xiàn)神經(jīng)再生速度比對(duì)照組快,，而沉默或敲除dlk-1基因,，神經(jīng)細(xì)胞徹底失去再生功能。進(jìn)一步研究表明dlk-1和其他三個(gè)基因一起調(diào)控整個(gè)神經(jīng)再生通路表達(dá),，此通路屬于MAPK信號(hào)通路,。dlk-1基因所表達(dá)的DLK-1蛋白在調(diào)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.
