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Nucleotide sequence of cauliflower mosaic virus DNA.花椰菜花叶病毒DNA的核苷酸序列。
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The influence of the microtubule inhibitor, methyl benzimidazol-2-yl-carbamate (MBC) on nuclear division and the cell cycle in Saccharomyces cerevisiae.微管抑制剂甲基苯并咪唑-2-基氨基甲酸酯(MBC)对酿酒酵母核分裂和细胞周期的影响。
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6
Rat monoclonal antitubulin antibodies derived by using a new nonsecreting rat cell line.通过使用一种新的非分泌型大鼠细胞系获得的大鼠抗微管蛋白单克隆抗体。
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BIK1是酿酒酵母交配和有丝分裂过程中微管功能所需的一种蛋白质,它与微管蛋白共定位。

BIK1, a protein required for microtubule function during mating and mitosis in Saccharomyces cerevisiae, colocalizes with tubulin.

作者信息

Berlin V, Styles C A, Fink G R

机构信息

Whitehead Institute for Biomedical Research, Cambridge, Massachusetts.

出版信息

J Cell Biol. 1990 Dec;111(6 Pt 1):2573-86. doi: 10.1083/jcb.111.6.2573.

DOI:10.1083/jcb.111.6.2573
PMID:2277073
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2116401/
Abstract

BIK1 function is required for nuclear fusion, chromosome disjunction, and nuclear segregation during mitosis. The BIK1 protein colocalizes with tubulin to the spindle pole body and mitotic spindle. Synthetic lethality observed in double mutant strains containing a mutation in the BIK1 gene and in the gene for alpha- or beta-tubulin is consistent with a physical interaction between BIK1 and tubulin. Furthermore, over- or underexpression of BIK1 causes aberrant microtubule assembly and function, bik1 null mutants are viable but contain very short or undetectable cytoplasmic microtubules. Spindle formation often occurs strictly within the mother cell, probably accounting for the many multinucleate and anucleate bik1 cells. Elevated levels of chromosome loss in bik1 cells are indicative of defective spindle function. Nuclear fusion is blocked in bik1 x bik1 zygotes, which have truncated cytoplasmic microtubules. Cells overexpressing BIK1 initially have abnormally short or nonexistent spindle microtubules and long cytoplasmic microtubules. Subsequently, cells lose all microtubule structures, coincident with the arrest of division. Based on these results, we propose that BIK1 is required stoichiometrically for the formation or stabilization of microtubules during mitosis and for spindle pole body fusion during conjugation.

摘要

在有丝分裂过程中,核融合、染色体分离和核分裂需要BIK1发挥功能。BIK1蛋白与微管蛋白共定位于纺锤极体和有丝分裂纺锤体。在含有BIK1基因突变以及α-或β-微管蛋白基因突变的双突变菌株中观察到的合成致死现象,与BIK1和微管蛋白之间的物理相互作用一致。此外,BIK1的过表达或低表达会导致微管组装和功能异常,bik1基因敲除突变体是可存活的,但含有非常短或无法检测到的细胞质微管。纺锤体形成通常严格发生在母细胞内,这可能是许多多核和无核bik1细胞产生的原因。bik1细胞中染色体丢失水平升高表明纺锤体功能存在缺陷。在具有截短细胞质微管的bik1×bik1合子中,核融合被阻断。过表达BIK1的细胞最初具有异常短或不存在的纺锤体微管以及长的细胞质微管。随后,细胞失去所有微管结构,同时细胞分裂停止。基于这些结果,我们提出在有丝分裂期间,BIK1在化学计量上是微管形成或稳定以及接合过程中纺锤极体融合所必需的。