Drosophila F-BAR protein Syndapin contributes to coupling the plasma membrane and contractile ring in cytokinesis

Drosophila F-BAR protein Syndapin contributes to coupling the plasma membrane and contractile ring in cytokinesis
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果蝇 F-BAR 蛋白 Syndapin 有助于胞质分裂中质膜和收缩环的耦合

DOI:
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发表时间:
2013
期刊:
影响因子:
5.8
通讯作者:
David M. Glover
David M. Glover
中科院分区:
生物学2区
文献类型:
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作者:
Tetsuya Takeda;Iain M. Robinson;Matthew M. Savoian;John R. Griffiths;Anthony D. Whetton;Harvey T Mcmahon;David M. Glover

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胞质分裂是一个高度有序的细胞过程,由中央纺锤体微管和肌动球蛋白收缩环之间的相互作用驱动,与质膜的动态重塑有关。在胞质分裂中,负责重组细胞赤道处的质膜及其与收缩环偶联的机制知之甚少。我们在这里报告,Syndapin,一种蛋白质含有膜曲率所需的F-BAR结构域,有助于重塑细胞质分裂收缩环周围的质膜。Syndapin与磷脂酰肌醇4,5-二磷酸(PI(4,5)P2)共定位在卵裂沟处,在那里它直接与收缩环组分Anilin相互作用。因此,在Syndapin突变体的胞质分裂期间,苯胺醛被错误定位。Syndapin的表达升高或降低导致胞质分裂缺陷伴异常皮质动力学。能够定位于卵裂沟并诱导胞质分裂缺陷的Syndapin的最小片段是F-BAR结构域及其紧邻的C-末端序列。该区域的磷酸化阻止了这种功能性相互作用,导致Syndapin结合膜和使膜变形的能力降低。因此,Syndapin的去磷酸化形式介导质膜的重塑及其与细胞动力学机制的适当偶联。
Cytokinesis is a highly ordered cellular process driven by interactions between central spindle microtubules and the actomyosin contractile ring linked to the dynamic remodelling of the plasma membrane. The mechanisms responsible for reorganizing the plasma membrane at the cell equator and its coupling to the contractile ring in cytokinesis are poorly understood. We report here that Syndapin, a protein containing an F-BAR domain required for membrane curvature, contributes to the remodelling of the plasma membrane around the contractile ring for cytokinesis. Syndapin colocalizes with phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) at the cleavage furrow, where it directly interacts with a contractile ring component, Anillin. Accordingly, Anillin is mislocalized during cytokinesis in Syndapin mutants. Elevated or diminished expression of Syndapin leads to cytokinesis defects with abnormal cortical dynamics. The minimal segment of Syndapin, which is able to localize to the cleavage furrow and induce cytokinesis defects, is the F-BAR domain and its immediate C-terminal sequences. Phosphorylation of this region prevents this functional interaction, resulting in reduced ability of Syndapin to bind to and deform membranes. Thus, the dephosphorylated form of Syndapin mediates both remodelling of the plasma membrane and its proper coupling to the cytokinetic machinery.
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