Hao Yan, Collins Catherine
Department of Molecular, Cellular, and Developmental Biology, University of Michigan, Ann Arbor, MI 48109-1048, USA.
Department of Molecular, Cellular, and Developmental Biology, University of Michigan, Ann Arbor, MI 48109-1048, USA.
Curr Opin Genet Dev. 2017 Jun;44:84-91. doi: 10.1016/j.gde.2017.01.009. Epub 2017 Feb 21.
Axonal damage and loss are common and negative consequences of neuronal injuries, and also occur in some neurodegenerative diseases. For neurons to have a chance to repair their connections, they need to survive the damage, initiate new axonal growth, and ultimately establish new synaptic connections. This review discusses how recent work in Drosophila models have informed our understanding of the cellular pathways used by neurons to respond to axonal injuries. Similarly to mammalian neurons, Drosophila neurons appear to be more limited in their capacity regrow (regenerate) damaged axons in the central nervous system, but can undergo axonal regeneration to varying extents in the peripheral nervous system. Conserved cellular pathways are activated by axonal injury via mechanisms that are specific to axons but not dendrites, and new unanticipated inhibitors of axon regeneration can be identified via genetic screening. These findings, made predominantly via genetic and live imaging methods in Drosophila, emphasize the utility of this model organism for the identification and study of basic cellular mechanisms used for neuronal repair.
轴突损伤和丢失是神经元损伤常见的负面后果，在一些神经退行性疾病中也会发生。为了使神经元有机会修复其连接，它们需要在损伤中存活下来，启动新的轴突生长，并最终建立新的突触连接。本综述讨论了果蝇模型中的最新研究如何增进我们对神经元用于应对轴突损伤的细胞途径的理解。与哺乳动物神经元类似，果蝇神经元在中枢神经系统中重新生长（再生）受损轴突的能力似乎更有限，但在外周神经系统中可以在不同程度上进行轴突再生。保守的细胞途径通过轴突特有的机制被轴突损伤激活，而不是树突，并且可以通过基因筛选鉴定新的意外的轴突再生抑制剂。这些主要通过果蝇中的遗传和实时成像方法得出的发现，强调了这种模式生物在识别和研究用于神经元修复的基本细胞机制方面的效用。
