PP6磷酸酶和伸长子通过控制微管调节因子的水平来促进激酶5依赖性纺锤体组装。

IF 3.7 2区 生物学 Q1 GENETICS & HEREDITY
Laura Marín, Jorge Castro-Sangrador, Marta Hoya, Shara Tello, Pedro M Coll, Javier Encinar Del Dedo, Alfonso Fernández-Álvarez, Juan C Ribas, Phong T Tran, Sergio A Rincon
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引用次数: 0

摘要

真核生物的染色体分离依赖于基于微管(MTs)的双极性机器的组装,称为有丝分裂纺锤体。有丝分裂纺锤体的形成遵循一种力平衡机制,确保姐妹染色单体的正确捕获和分离。许多蛋白质都参与了这种力平衡的建立,尽管运动蛋白5被认为是主要的向外推力的产生者,因为它的失活导致单极的、无功能的纺锤体。为了找到力平衡机制中的其他参与者,我们使用裂变酵母激酶5同源基因Cut7的条件等位基因进行了抑制筛选。该筛选发现,PP6磷酸酶的缺乏部分抑制了cut - 7表型,至少是由于MT调节因子(如负端定向驱动蛋白Klp2、MT稳定剂Alp7和MT捆绑剂Ase1)的翻译缺陷,影响了力平衡机制。此外,我们的数据显示,细长复合物,一个被PP6激活以进行有效tRNA修饰的靶标,也有助于力平衡,尽管程度较小。重要的是,这个复合体最近被认为与后生动物的直接MT聚合有关,这是它的裂变酵母对应物所没有的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
PP6 phosphatase and Elongator contribute to kinesin 5-dependent spindle assembly by controlling microtubule regulators levels.

Eukaryotic chromosome segregation relies on the assembly of a bipolar machinery based on microtubules (MTs), named the mitotic spindle. Formation of the mitotic spindle follows a force balance mechanism that ensures the proper capture and separation of sister chromatids. Many proteins have been involved in the establishment of this force balance, although kinesin 5 is well recognized as the major outward pushing force generator, since its inactivation results in monopolar, non-functional spindles. In order to find additional players in the force balance mechanism, we have performed a suppressor screen using a conditional allele of the fission yeast kinesin 5 ortholog Cut7. This screen identified that the lack of the PP6 phosphatase partially suppresses cut7 phenotypes, at least by defective translation of MT regulators, such as the minus end-directed kinesin Klp2, the MT stabilizer Alp7 and the MT bundler Ase1, impacting on the force balance mechanism. Additionally, our data show that the Elongator complex, a target activated by PP6 for efficient tRNA modification, also contributes to the force balance, albeit to a lesser extent. Importantly, this complex has recently been implicated in direct MT polymerization in metazoans, a role not shared by its fission yeast counterpart.

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来源期刊
PLoS Genetics
PLoS Genetics GENETICS & HEREDITY-
自引率
2.20%
发文量
438
期刊介绍: PLOS Genetics is run by an international Editorial Board, headed by the Editors-in-Chief, Greg Barsh (HudsonAlpha Institute of Biotechnology, and Stanford University School of Medicine) and Greg Copenhaver (The University of North Carolina at Chapel Hill). Articles published in PLOS Genetics are archived in PubMed Central and cited in PubMed.
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