Richardson Brian E, Nowak Scott J, Baylies Mary K
Sloan-Kettering Institute, Weill Graduate School of Medical Sciences, Cornell University, New York, NY 10021, USA.
Traffic. 2008 Jul;9(7):1050-9. doi: 10.1111/j.1600-0854.2008.00756.x. Epub 2008 Apr 24.
Muscle formation and repair depends critically on the fusion of myoblasts. Despite the importance of this process, little is known about the cellular and molecular mechanisms regulating fusion. Forward genetic screens in Drosophila melanogaster have uncovered genes that, when mutated, prevent myoblast fusion. Analyses of these gene products have indicated that the actin cytoskeleton and its regulation play a central role in the fusion process. In this review, we discuss recent advances in the field, including new imaging approaches to analyze fusion as well as a description of novel genes required for fusion. In particular, we highlight what has been learned about the requirement of a specific actin structure at the site of fusion. We also place these findings from Drosophila within the context of myoblast fusion in vertebrates.
肌肉的形成和修复严重依赖于成肌细胞的融合。尽管这一过程很重要,但对于调节融合的细胞和分子机制却知之甚少。在黑腹果蝇中进行的正向遗传学筛选发现了一些基因,这些基因发生突变时会阻止成肌细胞融合。对这些基因产物的分析表明,肌动蛋白细胞骨架及其调节在融合过程中起着核心作用。在这篇综述中,我们讨论了该领域的最新进展,包括用于分析融合的新成像方法以及对融合所需新基因的描述。特别地,我们强调了在融合位点对特定肌动蛋白结构的需求方面所学到的知识。我们还将果蝇的这些发现置于脊椎动物成肌细胞融合的背景中。