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Unraveling the mechanisms of synapse formation and axon regeneration: the awesome power of C. elegans genetics

机译:揭示突触形成和轴突再生的机制:秀丽隐杆线虫遗传学的强大力量

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Since Caenorhabditis elegans was chosen as a model organism by Sydney Brenner in 1960’s, genetic studies in this organism have been instrumental in discovering the function of genes and in deciphering molecular signaling network. The small size of the organism and the simple nervous system enable the complete reconstruction of the first connectome. The stereotypic developmental program and the anatomical reproducibility of synaptic connections provide a blueprint to dissect the mechanisms underlying synapse formation. Recent technological innovation using laser surgery of single axons and in vivo imaging has also made C. elegans a new model for axon regeneration. Importantly, genes regulating synaptogenesis and axon regeneration are highly conserved in function across animal phyla. This mini-review will summarize the main approaches and the key findings in understanding the mechanisms underlying the development and maintenance of the nervous system. The impact of such findings underscores the awesome power of C. elegans genetics. Keywords presynaptic active zone DLK kinase microtubule dynamics EFA-6 RPM-1 SYD-2 Liprin ubiquitin E3 ligase axon injury laser axotomy.
机译:自从秀丽隐杆线虫在1960年代被悉尼布伦纳(Sydney Brenner)选为模型生物以来,对该生物的遗传研究一直在发现基因的功能和破译分子信号网络方面发挥了作用。小巧的生物体和简单的神经系统可以完全重建第一个连接体。刻板印象的发展计划和突触连接的解剖学可再现性提供了一个蓝图来剖析突触形成基础的机制。使用单轴突的激光手术和体内成像的最新技术创新也使秀丽隐杆线虫成为轴突再生的新模型。重要的是,调节突触发生和轴突再生的基因在整个动物门的功能上高度保守。这份小型回顾将总结理解神经系统发育和维持机制的主要方法和关键发现。这些发现的影响强调了秀丽隐杆线虫遗传学的强大功能。关键词突触前活动区DLK激酶微管动力学EFA-6 RPM-1 SYD-2脂蛋白泛素E3连接酶轴突损伤激光轴切。

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