首页> 美国卫生研究院文献>Genetics >Overexpression of Yeast Homologs of the Mammalian Checkpoint Gene Rcc1 Suppresses the Class of α-Tubulin Mutations That Arrest with Excess Microtubules
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Overexpression of Yeast Homologs of the Mammalian Checkpoint Gene Rcc1 Suppresses the Class of α-Tubulin Mutations That Arrest with Excess Microtubules

机译:酵母检查点基因Rcc1的酵母同系物的过表达抑制一类微管多余的α-Tubulin突变。

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摘要

Microtubules in eukaryotic cells participate in a variety of nuclear and cytoplasmic structures, reflecting functional requirements and cell cycle position. We are studying the cellular regulation of microtubule assembly and organization in the yeast Saccharomyces cerevisiae. We screened for genes that when overexpressed suppress the growth phenotype of conditional mutants in α-tubulin that arrest with excess microtubules at the nonpermissive temperature (class 2 mutations). Here we describe one such suppressing element, called ATS1 (for Alpha Tubulin Suppressor). Overexpression of this gene rescues both the growth and microtubule phenotypes of all class 2 mutations, but not the cold-sensitive mutations that arrest with no microtubules (class 1 mutations). Deletion of ATS1 confers a modest slow growth phenotype which is slightly enhanced in strains containing both a deletion of ATS1 and a class 2 tub1 mutation. The predicted ATS1 protein contains 333 amino acids and has considerable structural homology to the products of both the mammalian mitotic control gene RCC1 and the S. cerevisiae gene SRM1/PRP20. Overexpression of SRM1/PRP20 also suppresses class 2 mutants. The results suggest that this family of genes may participate in regulatory interactions between microtubules and the cell cycle.
机译:真核细胞中的微管参与各种核和细胞质结构,反映了功能要求和细胞周期位置。我们正在研究啤酒酵母中微管组装和组织的细胞调节。我们筛选了过表达抑制α-微管蛋白中条件性突变体的生长表型的基因,该条件性突变体在非允许温度下因过量的微管而停滞(2类突变)。在这里,我们描述了一种这样的抑制元件,称为ATS1(用于Alpha Tubulin抑制剂)。该基因的过表达可以挽救所有2类突变的生长和微管表型,但不能挽救没有微管的冷敏感突变(1类突变)。 ATS1的删除赋予适度的缓慢生长表型,在包含ATS1缺失和2类tub1突变的菌株中,这种表型会稍有增强。预测的ATS1蛋白含有333个氨基酸,并且与哺乳动物的有丝分裂控制基因RCC1和酿酒酵母基因SRM1 / PRP20的产物具有相当的结构同源性。 SRM1 / PRP20的过表达也抑制了2类突变体。结果表明该基因家族可能参与微管与细胞周期之间的调控相互作用。

著录项

  • 期刊名称 Genetics
  • 作者

    D. Kirkpatrick; F. Solomon;

  • 作者单位
  • 年(卷),期 1994(137),2
  • 年度 1994
  • 页码 381–392
  • 总页数 12
  • 原文格式 PDF
  • 正文语种
  • 中图分类 遗传学;
  • 关键词

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