Lu K P, Hunter T
Molecular Biology and Virology Laboratory, Salk Institute, La Jolla, California 92037, USA.
Cell. 1995 May 5;81(3):413-24. doi: 10.1016/0092-8674(95)90394-1.
NIMA is essential for entry into mitosis in Aspergillus nidulans. To examine whether there is a NIMA-like pathway in other eukaryotic cell cycles, we expressed NIMA and its dominant negative mutants in two different eukaryotic systems. In Xenopus oocytes, NIMA induced germinal vesicle breakdown without activating Mos, CDC2, or MAP kinase. In HeLa cells, NIMA induced premature mitotic events without activating CDC2, whereas the mutants caused a specific G2 arrest but did not block mutant CDC2T14AY15F-induced premature entry into mitosis. A sequence essential for both these phenotypes was mapped to a region of approximately 100 amino acids lying just after the catalytic domain of NIMA that shows a significant similarity to protein interaction domains in other proteins. These results provide evidence for the existence of a NIMA-like mitotic pathway in vertebrate cells.
NIMA对于构巢曲霉进入有丝分裂至关重要。为了研究在其他真核细胞周期中是否存在类似NIMA的途径，我们在两种不同的真核系统中表达了NIMA及其显性负突变体。在非洲爪蟾卵母细胞中，NIMA诱导生发泡破裂，而不激活Mos、CDC2或丝裂原活化蛋白激酶。在HeLa细胞中，NIMA诱导过早的有丝分裂事件，而不激活CDC2，而突变体导致特异性的G2期阻滞，但不阻断突变型CDC2T14AY15F诱导的过早进入有丝分裂。这两种表型所必需的序列被定位到NIMA催化结构域之后约100个氨基酸的区域，该区域与其他蛋白质中的蛋白质相互作用结构域具有显著相似性。这些结果为脊椎动物细胞中存在类似NIMA的有丝分裂途径提供了证据。
