Shirayama M, Matsui Y, Tanaka K, Toh-e A
Department of Biology, Faculty of Science, University of Tokyo, Japan.
Yeast. 1994 Apr;10(4):451-61. doi: 10.1002/yea.320100404.
We have identified MSI2 as a gene of Saccharomyces cerevisiae which, when on a multicopy vector, suppresses the heat shock sensitivity caused by the loss of the IRA1 product, a negative regulator of the RAS protein. The multicopy MSI2 also suppresses the heat shock sensitivity of cells with the RAS2val19 mutation but not those with the bcy1 mutation, suggesting that the MSI2 protein may interfere with the activity of the RAS protein. The sequence analysis of MSI2 reveals that it is identical to LTE1 belonging to the CDC25 family: CDC25, SCD25 and BUD5, each of which encodes a guanine nucleotide exchange factor for the ras superfamily gene products. Deletion of the entire MSI2 coding region reveals that MSI2 is not essential but the disruptant shows a cold-sensitive phenotype. Under the non-permissive conditions, more than 70% of the msi2 disruptants arrested at telophase as large budded cells with two nuclei divided completely and elongated spindles, indicating that the msi2 deletion is a cell division cycle mutation. These results suggest that MSI2 is involved in the termination of M phase and that this process is regulated by a ras superfamily gene product.
我们已确定MSI2是酿酒酵母的一个基因，当它存在于多拷贝载体上时，可抑制由IRA1产物缺失引起的热休克敏感性，IRA1产物是RAS蛋白的负调节因子。多拷贝的MSI2也可抑制具有RAS2val19突变的细胞的热休克敏感性，但不能抑制具有bcy1突变的细胞的热休克敏感性，这表明MSI2蛋白可能会干扰RAS蛋白的活性。对MSI2的序列分析表明，它与属于CDC25家族的LTE1相同：CDC25、SCD25和BUD5，它们各自编码一种针对ras超家族基因产物的鸟嘌呤核苷酸交换因子。删除整个MSI2编码区表明，MSI2并非必需，但破坏株表现出冷敏感表型。在非允许条件下，超过70%的msi2破坏株在末期停滞，成为具有两个完全分开的细胞核和伸长纺锤体的大芽殖细胞，这表明msi2缺失是一种细胞分裂周期突变。这些结果表明，MSI2参与M期的终止，并且该过程受ras超家族基因产物的调节。
