Schaerer-Brodbeck C, Riezman H
Biozentrum of the University of Basel, Klingelbergstrasse 70, CH-4056 Basel, Switzerland.
J Cell Sci. 2000 Feb;113 ( Pt 3):521-32. doi: 10.1242/jcs.113.3.521.
Analysis of the arc35-1 mutant has revealed previously that this component of the Arp2/3 complex is involved in organization of the actin cytoskeleton. Further characterization uncovered a cell division cycle phenotype with arrest as large-budded cells. Cells with correctly positioned metaphase spindles accumulated at the restrictive temperature. The observed metaphase arrest most likely occurs by activation of the spindle assembly checkpoint, because arc35-1 was synthetically lethal with a deletion of BUB2. Arc35p activity is required late in G(1) for its cell cycle function. Both the actin and microtubule defects of arc35-1 can be suppressed by overexpression of calmodulin. Analysis of a collection of ts cmd1 mutants for their ability to suppress the actin and/or microtubule defect revealed that the two defects observed in arc35-1 are genetically separable. These data suggest that the actin defect is probably not the cause of the microtubule defect.
对arc35-1突变体的分析先前已揭示，Arp2/3复合物的这一组成部分参与肌动蛋白细胞骨架的组织。进一步的表征发现了一种细胞分裂周期表型，即细胞停滞在大芽期。在限制温度下，中期纺锤体定位正确的细胞会积累。观察到的中期停滞很可能是通过纺锤体组装检查点的激活而发生的，因为arc35-1与BUB2缺失具有合成致死性。Arc35p活性在G(1)晚期是其细胞周期功能所必需的。钙调蛋白的过表达可以抑制arc35-1的肌动蛋白和微管缺陷。对一组温度敏感的cmd1突变体抑制肌动蛋白和/或微管缺陷能力的分析表明，在arc35-1中观察到的两种缺陷在遗传上是可分离的。这些数据表明，肌动蛋白缺陷可能不是微管缺陷的原因。
