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formin 节点和肌球蛋白马达活性在有丝分裂酵母胞质分裂中期依赖 Mid1p 的收缩环组装中的作用。

Roles of formin nodes and myosin motor activity in Mid1p-dependent contractile-ring assembly during fission yeast cytokinesis.

机构信息

Department of Molecular Genetics, Graduate Program of Molecular, Cellular, and Developmental Biology, The Ohio State University, Columbus, OH 43210, USA.

出版信息

Mol Biol Cell. 2009 Dec;20(24):5195-210. doi: 10.1091/mbc.e09-05-0428.

DOI:10.1091/mbc.e09-05-0428
PMID:19864459
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2793295/
Abstract

Two prevailing models have emerged to explain the mechanism of contractile-ring assembly during cytokinesis in the fission yeast Schizosaccharomyces pombe: the spot/leading cable model and the search, capture, pull, and release (SCPR) model. We tested some of the basic assumptions of the two models. Monte Carlo simulations of the SCPR model require that the formin Cdc12p is present in >30 nodes from which actin filaments are nucleated and captured by myosin-II in neighboring nodes. The force produced by myosin motors pulls the nodes together to form a compact contractile ring. Live microscopy of cells expressing Cdc12p fluorescent fusion proteins shows for the first time that Cdc12p localizes to a broad band of 30-50 dynamic nodes, where actin filaments are nucleated in random directions. The proposed progenitor spot, essential for the spot/leading cable model, usually disappears without nucleating actin filaments. alpha-Actinin ain1 deletion cells form a normal contractile ring through nodes in the absence of the spot. Myosin motor activity is required to condense the nodes into a contractile ring, based on slower or absent node condensation in myo2-E1 and UCS rng3-65 mutants. Taken together, these data provide strong support for the SCPR model of contractile-ring formation in cytokinesis.

摘要

两种流行的模型已经出现来解释有丝分裂酵母裂殖酵母细胞分裂过程中收缩环组装的机制

点/主导索模型和搜索、捕获、拉动和释放 (SCPR) 模型。我们测试了这两个模型的一些基本假设。SCPR 模型的蒙特卡罗模拟要求formin Cdc12p 存在于 30 个以上的节点中,肌球蛋白-II 可以从这些节点起始并捕获肌动蛋白丝。肌球蛋白马达产生的力将节点拉到一起形成一个紧凑的收缩环。首次通过表达 Cdc12p 荧光融合蛋白的活细胞显微镜观察表明,Cdc12p 定位于 30-50 个动态节点的宽带上,肌动蛋白丝在这些节点中随机起始。对于点/主导索模型至关重要的前体点通常在没有起始肌动蛋白丝的情况下消失。由于缺乏点,肌动蛋白 ain1 缺失细胞通过节点形成正常的收缩环。基于肌球蛋白 II 突变体 myo2-E1 和 UCS rng3-65 中较慢或不存在的节点浓缩,肌球蛋白马达活性对于将节点浓缩成收缩环是必需的。总的来说,这些数据为 SCPR 模型在有丝分裂中的收缩环形成提供了强有力的支持。

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本文引用的文献

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Regulation of fission yeast myosin-II function and contractile ring dynamics by regulatory light-chain and heavy-chain phosphorylation.通过调节轻链和重链磷酸化对裂殖酵母肌球蛋白-II功能及收缩环动力学的调控
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Mid1p/anillin and the septation initiation network orchestrate contractile ring assembly for cytokinesis.Mid1p/缢缩蛋白和隔膜起始网络协调收缩环组装以进行胞质分裂。
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The cytokinesis formins from the nematode worm and fission yeast differentially mediate actin filament assembly.来自线虫和裂殖酵母的胞质分裂formin蛋白差异介导肌动蛋白丝组装。
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Yeast UCS proteins promote actomyosin interactions and limit myosin turnover in cells.酵母UCS蛋白促进细胞中的肌动球蛋白相互作用并限制肌球蛋白更新。
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Progress towards understanding the mechanism of cytokinesis in fission yeast.在理解裂殖酵母胞质分裂机制方面取得的进展。
Biochem Soc Trans. 2008 Jun;36(Pt 3):425-30. doi: 10.1042/BST0360425.