Desnos Claire, Huet Sébastien, Darchen François
Institut de Biologie Physico-Chimique, Centre National de la Recherche Scientifique, UPR 1929, Université Paris 7 Denis Diderot, Paris, France.
Biol Cell. 2007 Aug;99(8):411-23. doi: 10.1042/BC20070021.
Actin- and microtubule-based motors can propel different cargos along filaments. Within cells, they control the distribution of membrane-bound compartments by performing complementary tasks. Organelles make long journeys along microtubules, with class V myosins ensuring their capture and their dispersal in actin-rich regions. Myosin Va is recruited on to diverse organelles, such as melanosomes and secretory vesicles, by a mechanism involving Rab GTPases. The role of myosin Va in the recruitment of secretory vesicles at the plasma membrane reveals that the cortical actin network cannot merely be seen as a physical barrier hindering vesicle access to release sites. In neurons, myosin Va controls the targeting of IP(3) (inositol 1,4,5-trisphosphate)-sensitive Ca(2+) stores to dendritic spines and the transport of mRNAs. These defects probably account for the severe neurological symptoms observed in Griscelli syndrome due to mutations in the MYO5A gene.
基于肌动蛋白和微管的分子马达能够沿着细丝推动不同的货物。在细胞内,它们通过执行互补任务来控制膜结合区室的分布。细胞器沿着微管进行长距离运输,V类肌球蛋白确保它们在富含肌动蛋白的区域被捕获并分散。肌球蛋白Va通过一种涉及Rab GTP酶的机制被招募到各种细胞器上,如黑素小体和分泌囊泡。肌球蛋白Va在质膜上分泌囊泡招募过程中的作用表明,皮质肌动蛋白网络不能仅仅被视为阻碍囊泡进入释放位点的物理屏障。在神经元中,肌球蛋白Va控制IP(3)(肌醇1,4,5-三磷酸)敏感的Ca(2+)储存库向树突棘的靶向运输以及mRNA的运输。这些缺陷可能是由于MYO5A基因突变导致的格里塞利综合征中观察到的严重神经症状的原因。