Fragile Axons Forge the Path to Gene Discovery: A MAP Kinase Pathway Regulates Axon Regeneration
Fragile Axons Forge the Path to Gene Discovery: A MAP Kinase Pathway Regulates Axon Regeneration
复制标题
脆弱的轴突开辟了基因发现之路：MAP 激酶途径调节轴突再生
作者：
Georgeann S. O’Brien;A. Sagasti
在秀丽隐杆线虫中，有丝分裂原激活的蛋白激酶途径是再生而不是发育性轴突生长所必需的。秀丽隐杆线虫是研究轴突再生分子控制的一个有前途的模型。正向遗传筛选发现DLK-1（双亮氨酸拉链-轴承激酶1）MAP（丝裂原活化蛋白）激酶途径是轴突再生过程中生长锥形成的积极调节因子。虽然DLK-1通路突变动物在再生中表现出显著缺陷，但它们的轴突在最初的生长中没有明显缺陷。DLK-1通路也在突触发生中起作用，但这一作用似乎与其在再生中的功能是分开的。了解DLK-1通路在发育、可塑性和再生中的作用，可能有助于揭示调节轴突再生机制的进化。
In Caenorhabditis elegans, a mitogen-activated protein kinase pathway is required for regenerative but not developmental axon outgrowth. The nematode Caenorhabditis elegans is emerging as a promising model for studying the molecular control of axon regeneration. A forward genetic screen identified the DLK-1 (dual leucine zipper-bearing kinase 1) MAP (mitogen-activated protein) kinase pathway as a positive regulator of growth cone formation during axon regeneration. Although DLK-1 pathway mutant animals display a dramatic defect in regeneration, their axons have no apparent defects in initial outgrowth. The DLK-1 pathway also plays a role in synaptogenesis, but this role appears to be separate from its function in regeneration. Understanding how the DLK-1 pathway acts in development, plasticity, and regeneration may shed light on the evolution of mechanisms regulating axon regeneration.