Nuf, a Rab11 effector, maintains cytokinetic furrow integrity by promoting local actin polymerization.
Nuf, a Rab11 effector, maintains cytokinetic furrow integrity by promoting local actin polymerization.
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DOI：
10.1083/jcb.200712036
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发表时间：
2008-07-28
期刊：
影响因子：
--
通讯作者：
Sullivan W
中科院分区：
文献类型：
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作者：
Cao J;Albertson R;Riggs B;Field CM;Sullivan W
胞质分裂过程中的质膜内移涉及肌动蛋白重塑和囊泡介导的膜添加。从再循环内体（RE）的囊泡为基础的膜递送在胞质分裂中具有重要但不明确的参与。在果蝇早期胚胎中，NUF（核沉降），Rab 11效应是RE功能所必需的，是必需的F-肌动蛋白和膜的完整性在沟内进。我们发现，在nuf突变体胚胎，最初的损失F-肌动蛋白在犁沟的损失，其次是相关的犁沟膜。用Latrunculin A或Rho抑制剂处理的野生型胚胎显示出类似的缺陷。药物或Rho-GTP诱导的肌动蛋白聚合的增加或遗传介导的肌动蛋白解聚的减少抑制了nuf突变体F-肌动蛋白和膜缺陷。我们还发现，RhoGEF 2没有正确定位在nuf突变体胚胎的犁沟，RhoGEF 2-Rho 1通路组件显示出强烈的特异性遗传相互作用与Nuf。我们提出了一个模型，其中RE衍生的囊泡通过调节肌动蛋白聚合速率通过RhoGEF 2-Rho 1途径促进沟的完整性。
Plasma membrane ingression during cytokinesis involves both actin remodeling and vesicle-mediated membrane addition. Vesicle-based membrane delivery from the recycling endosome (RE) has an essential but ill-defined involvement in cytokinesis. In the Drosophila melanogaster early embryo, Nuf (Nuclear fallout), a Rab11 effector which is essential for RE function, is required for F-actin and membrane integrity during furrow ingression. We find that in nuf mutant embryos, an initial loss of F-actin at the furrow is followed by loss of the associated furrow membrane. Wild-type embryos treated with Latrunculin A or Rho inhibitor display similar defects. Drug- or Rho-GTP–induced increase of actin polymerization or genetically mediated decrease of actin depolymerization suppresses the nuf mutant F-actin and membrane defects. We also find that RhoGEF2 does not properly localize at the furrow in nuf mutant embryos and that RhoGEF2–Rho1 pathway components show strong specific genetic interactions with Nuf. We propose a model in which RE-derived vesicles promote furrow integrity by regulating the rate of actin polymerization through the RhoGEF2–Rho1 pathway.