Shirayama M, Matsui Y, Toh-E A
Department of Biology, University of Tokyo, Japan.
Mol Cell Biol. 1994 Nov;14(11):7476-82. doi: 10.1128/mcb.14.11.7476-7482.1994.
LTE1 belongs to the CDC25 family that encodes a guanine nucleotide exchange factor for GTP-binding proteins of the ras family. Previously we have shown that LTE1 is essential for termination of M phase at low temperatures. We have identified TEM1 as a gene that, when present on a multicopy plasmid, suppresses the cold-sensitive phenotype of lte1. Sequence analysis of TEM1 and GTP-binding analysis of the gene product revealed that TEM1 encodes a novel low-molecular-weight GTP-binding protein. The defect of TEM1 was lethal, and the tem1-defective cells were arrested at telophase with high H1-kinase activity under restrictive conditions, indicating that TEM1 is required to exit from M phase. The defect of TEM1 was suppressed by a high dose of CDC15, which encodes a protein kinase homologous to mitogen-activated protein kinase kinase kinases. The genetic interaction among LTE1, TEM1, and CDC15 indicates that they cooperatively play an essential role for termination of M phase.
LTE1属于CDC25家族，该家族编码一种针对ras家族GTP结合蛋白的鸟嘌呤核苷酸交换因子。此前我们已经表明，LTE1在低温下对M期的终止至关重要。我们已将TEM1鉴定为一个基因，当它存在于多拷贝质粒上时，可抑制lte1的冷敏感表型。TEM1的序列分析及其基因产物的GTP结合分析表明，TEM1编码一种新型低分子量GTP结合蛋白。TEM1缺陷是致死性的，在限制条件下，tem1缺陷细胞在末期因高H1激酶活性而停滞，这表明TEM1是退出M期所必需的。高剂量的CDC15可抑制TEM1的缺陷，CDC15编码一种与丝裂原活化蛋白激酶激酶激酶同源的蛋白激酶。LTE1、TEM1和CDC15之间的遗传相互作用表明，它们共同对M期的终止发挥重要作用。
