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肌动蛋白结合蛋白和隔膜蛋白促进胞质分裂沟的不对称内陷。

Anillin and the septins promote asymmetric ingression of the cytokinetic furrow.

作者信息

Maddox Amy Shaub, Lewellyn Lindsay, Desai Arshad, Oegema Karen

机构信息

Ludwig Institute for Cancer Research, Department of Cellular and Molecular Medicine (UCSD), CMM-East Rm. 3053, 9500 Gilman Drive, La Jolla, CA 92093, USA.

出版信息

Dev Cell. 2007 May;12(5):827-35. doi: 10.1016/j.devcel.2007.02.018.

DOI:10.1016/j.devcel.2007.02.018
PMID:17488632
Abstract

During cytokinesis, constriction of a cortical contractile ring generates a furrow that partitions one cell into two. The contractile ring contains three filament systems: actin, bipolar myosin II filaments, and septins, GTP-binding hetero-oligomers that polymerize to form a membrane-associated lattice. The contractile ring also contains a potential filament crosslinker, Anillin, that binds all three filament types. Here, we show that the contractile ring possesses an intrinsic symmetry-breaking mechanism that promotes asymmetric furrowing. Asymmetric ingression requires Anillin and the septins, which promote the coalescence of components on one side of the contractile ring, but is insensitive to a 10-fold reduction in myosin II levels. When asymmetry is disrupted, cytokinesis becomes sensitive to partial inhibition of contractility. Thus, asymmetric furrow ingression, a prevalent but previously unexplored feature of cell division in metazoans, is generated by the action of two conserved furrow components and serves a mechanical function that makes cytokinesis robust.

摘要

在胞质分裂过程中,皮层收缩环的收缩产生一个沟,将一个细胞分成两个。收缩环包含三种细丝系统:肌动蛋白、双极肌球蛋白II细丝和隔膜蛋白,后者是聚合形成膜相关晶格的GTP结合异源寡聚体。收缩环还包含一种潜在的细丝交联剂——膜收缩蛋白,它能结合所有三种细丝类型。在这里,我们表明收缩环具有一种内在的对称破坏机制,可促进不对称沟陷。不对称内陷需要膜收缩蛋白和隔膜蛋白,它们促进收缩环一侧成分的聚结,但对肌球蛋白II水平降低10倍不敏感。当不对称性被破坏时,胞质分裂对收缩性的部分抑制变得敏感。因此,不对称沟陷是后生动物细胞分裂中一个普遍但以前未被探索的特征,它由两种保守的沟成分的作用产生,并起到使胞质分裂稳健的机械功能。

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