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一种新型的检查点通路控制有丝分裂酵母中肌动球蛋白环收缩的触发。

A novel checkpoint pathway controls actomyosin ring constriction trigger in fission yeast.

机构信息

Instituto de Biología Funcional y Genómica, CSIC/Universidad de Salamanca and Departamento de Microbiología y Genética, Universidad de Salamanca, Salamanca, Spain.

出版信息

Elife. 2020 Oct 26;9:e59333. doi: 10.7554/eLife.59333.

Abstract

In fission yeast, the septation initiation network (SIN) ensures temporal coordination between actomyosin ring (CAR) constriction with membrane ingression and septum synthesis. However, questions remain about CAR regulation under stress conditions. We show that Rgf1p (Rho1p GEF), participates in a delay of cytokinesis under cell wall stress (blankophor, BP). BP did not interfere with CAR assembly or the rate of CAR constriction, but did delay the onset of constriction in the wild type cells but not in the Δ cells. This delay was also abolished in the absence of Pmk1p, the MAPK of the cell integrity pathway (CIP), leading to premature abscission and a multi-septated phenotype. Moreover, cytokinesis delay correlates with maintained SIN signaling and depends on the SIN to be achieved. Thus, we propose that the CIP participates in a checkpoint, capable of triggering a CAR constriction delay through the SIN pathway to ensure that cytokinesis terminates successfully.

摘要

在裂殖酵母中,隔膜起始网络(SIN)确保肌动球蛋白环(CAR)收缩与膜内陷和隔膜合成之间的时间协调。然而,关于应激条件下 CAR 调节的问题仍然存在。我们表明,Rgf1p(Rho1p GEF)参与细胞壁应激下的细胞分裂延迟(空白体,BP)。BP 不干扰 CAR 组装或 CAR 收缩的速度,但会延迟野生型细胞的收缩开始,但不会延迟Δ细胞的收缩开始。在不存在细胞完整性途径(CIP)的 MAPK Pmk1p 的情况下,这种延迟也被消除,导致过早分离和多分隔表型。此外,细胞分裂延迟与维持的 SIN 信号相关,并取决于 SIN 的实现。因此,我们提出 CIP 参与检查点,能够通过 SIN 途径触发 CAR 收缩延迟,以确保细胞分裂成功终止。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f22c/7661037/85e1155f4e8c/elife-59333-fig1.jpg

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