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原肌球蛋白1诱导的胞质分裂缺陷可通过提高丝切蛋白的表达来挽救。

A tropomyosin 1 induced defect in cytokinesis can be rescued by elevated expression of cofilin.

作者信息

Thoms Julie A I, Loch Heather M, Bamburg James R, Gunning Peter W, Weinberger Ron P

机构信息

Oncology Research Unit, The Children's Hospital at Westmead, Westmead, New South Wales, Australia.

出版信息

Cell Motil Cytoskeleton. 2008 Dec;65(12):979-90. doi: 10.1002/cm.20320.

Abstract

Cytokinesis in eukaryotic cells is mediated by the contractile ring, an actomyosin-based structure which provides the force required to separate daughter cells. Isoforms of the actin-binding protein tropomyosin are also localised to the contractile ring in both fission yeast and human astrocytes. Although tropomyosin is required for cytokinesis in yeast, its precise role in the contractile ring is unknown. In this study we find that increased expression of a single tropomyosin isoform, tropomyosin 1, in U373MG astrocytoma cells leads to multinucleated cells and mitotic spindle defects. Furthermore, cells expressing increased levels of tropomyosin 1 usually fail to complete cytokinesis and this is accompanied by reduced accumulation of actin depolymerising factor/cofilin in the contractile ring. Adenovirus mediated expression of cofilin is able to relieve the tropomyosin 1 induced effects on cytokinesis. We conclude that tropomyosin 1 and cofilin play antagonistic roles within the contractile ring and that the balance between tropomyosin 1 and cofilin expression is important for cytokinesis.

摘要

真核细胞中的胞质分裂由收缩环介导,收缩环是一种基于肌动球蛋白的结构,为分离子细胞提供所需的力。肌动蛋白结合蛋白原肌球蛋白的同工型也定位于裂殖酵母和人类星形胶质细胞的收缩环。虽然原肌球蛋白是酵母胞质分裂所必需的,但其在收缩环中的精确作用尚不清楚。在本研究中,我们发现U373MG星形细胞瘤细胞中单一原肌球蛋白同工型原肌球蛋白1的表达增加会导致多核细胞和有丝分裂纺锤体缺陷。此外,表达原肌球蛋白1水平升高的细胞通常无法完成胞质分裂,同时收缩环中肌动蛋白解聚因子/丝切蛋白的积累减少。腺病毒介导的丝切蛋白表达能够缓解原肌球蛋白1对胞质分裂的诱导作用。我们得出结论,原肌球蛋白1和丝切蛋白在收缩环中发挥拮抗作用,原肌球蛋白1和丝切蛋白表达之间的平衡对胞质分裂很重要。

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