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一种与正常核形态和染色体稳定性有关的进化保守的裂殖酵母蛋白Ned1,与Dis3、Pim1/RCC1和一种必需的核孔蛋白相互作用。

An evolutionarily conserved fission yeast protein, Ned1, implicated in normal nuclear morphology and chromosome stability, interacts with Dis3, Pim1/RCC1 and an essential nucleoporin.

作者信息

Tange Yoshie, Hirata Aiko, Niwa Osami

机构信息

Kazusa DNA Research Institute, 2-6-7 Kazusa-kamatari, Kisarazu, Chiba 292-0818, Japan.

出版信息

J Cell Sci. 2002 Nov 15;115(Pt 22):4375-85. doi: 10.1242/jcs.00135.

Abstract

We identified a novel fission yeast gene, ned1(+), with pleiotropic mutations that have a high incidence of chromosome missegregation, aberrantly shaped nuclei, overdeveloped endoplasmic reticulum-like membranes, and increased sensitivity to a microtubule destabilizing agent. Ned1 protein, which was phosphorylated in a growth-related manner, interacted in a yeast two-hybrid system with Dis3 as well as with Pim1/RCC1 (nucleotide exchange factor for Ran). Ned1 also interacted with an essential nucleoporin, a probable homologue of mammalian Nup98/96. The ned1 gene displayed a variety of genetic interactions with factors involved in nuclear transport and chromosome segregation, including the crm1 (exportin), spi1 (small GTPase Ran), pim1, and dis genes. A substitution mutation that affected the two-hybrid interaction with Dis3 increased chromosome instability, suggesting the functional importance of the interaction. Overproduction of Ned1 protein induced formation of an abnormal microtubule bundle within the nucleus, apparently independently of the spindle pole body, but dependent on pim1(+) activity. The ned1(+) gene belongs to an evolutionarily conserved gene family, which includes the mouse Lpin genes, one of whose mutations is responsible for lipodystrophy.

摘要

我们鉴定出一个新的裂殖酵母基因ned1(+),其多效性突变具有染色体错分离、细胞核形状异常、内质网样膜过度发育以及对微管去稳定剂敏感性增加的高发生率。以与生长相关的方式磷酸化的Ned1蛋白,在酵母双杂交系统中与Dis3以及Pim1/RCC1(Ran的核苷酸交换因子)相互作用。Ned1还与一种必需的核孔蛋白相互作用,该蛋白可能是哺乳动物Nup98/96的同源物。ned1基因与参与核转运和染色体分离的因子表现出多种遗传相互作用,包括crm1(输出蛋白)、spi1(小GTP酶Ran)、pim1和dis基因。影响与Dis3的双杂交相互作用的替代突变增加了染色体不稳定性,表明这种相互作用的功能重要性。Ned1蛋白的过量表达诱导细胞核内形成异常的微管束,显然独立于纺锤极体,但依赖于pim1(+)活性。ned1(+)基因属于一个进化上保守的基因家族,其中包括小鼠Lpin基因,其突变之一与脂肪营养不良有关。

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