Tanaka S, Nojima H
Department of Molecular Genetics, Research Institute for Microbial Diseases, Osaka University, Suita City, Japan.
Genes Cells. 1996 Oct;1(10):905-21. doi: 10.1046/j.1365-2443.1996.d01-213.x.
The eukaryotic cell cycle is driven by CDK-cyclin complexes. A number of proteins interact either with CDK or the CDK complex to regulate CDK activity. A search for novel cell cycle regulators in the budding yeast Saccharomyces cerevisiae yielded multicopy suppressors of the cdc2-L7 mutation of the fission yeast, Schizosaccharomyces pombe.
One of the isolated genes was found to encode a putative protein kinase similar to Nim1 of S. pombe and was termed NIK1 (Nim1-like kinase 1). Transcription of NIK1 was periodic and peaked at the G1/S boundary. Although NIK1 is not essential, delta nik1 cells showed G2 delay and hydroxyurea (HU) sensitivity. Anomalously elongated buds were observed in the stationary phase or in the presence of HU. Moreover, DNA was aberrantly distributed in the delta nik1 cdc28 double mutant. Genetical and biochemical evidence suggests that Nik1 interacts with the Cdc28 complex.
Nik is a structural and functional homologue of Nim1. Nik1 interacts with the Cdc28 complex and functions not only at the G2/M transition but also at other points of the cell cycle.
真核细胞周期由细胞周期蛋白依赖性激酶（CDK）-细胞周期蛋白复合物驱动。许多蛋白质与CDK或CDK复合物相互作用以调节CDK活性。在芽殖酵母酿酒酵母中寻找新型细胞周期调节因子时，发现了裂殖酵母粟酒裂殖酵母cdc2-L7突变的多拷贝抑制子。
发现其中一个分离基因编码一种与粟酒裂殖酵母的Nim1相似的假定蛋白激酶，被命名为NIK1（Nim1样激酶1）。NIK1的转录是周期性的，在G1/S边界达到峰值。虽然NIK1不是必需的，但缺失NIK1的细胞表现出G2期延迟和对羟基脲（HU）敏感。在稳定期或存在HU的情况下观察到异常伸长的芽。此外，在缺失NIK1的cdc28双突变体中DNA分布异常。遗传和生化证据表明Nik1与Cdc28复合物相互作用。
Nik是NimI的结构和功能同源物。Nik1与Cdc28复合物相互作用，不仅在G2/M转换期起作用，而且在细胞周期的其他阶段也起作用。
