Lu K P, Hunter T
Molecular Biology and Virology Laboratory, Salk Institute, La Jolla, California 92037, USA.
Prog Cell Cycle Res. 1995;1:187-205. doi: 10.1007/978-1-4615-1809-9_15.
CDC2 has been shown to regulate entry into mitosis in eukaryotic cells. However, in Aspergillus nidulans, activation of CDC2 itself is not sufficient to trigger mitosis if another mitotic protein kinase, NIMA, is not activated. Superficially, NIMA and CDC2 have analogous functions and are regulated in a similar manner. NIMA activity is tightly regulated during the cell cycle. Overexpression of NIMA induces germinal vesicle breakdown in Xenopus oocytes and promotes premature entry into mitosis in all eukaryotic cells examined, whereas dominant-negative mutant NIMA causes a specific G2 arrest in Aspergillus nidulans and human cells, as is the case for CDC2. However, NIMA and CDC2 have quite distinct primary sequence substrate specificities. Furthermore, the regulatory mechanisms that govern the cell cycle-dependent abundance, activity and localization are largely intramolecular for NIMA but intermolecular for CDC2. More importantly, a NIMA-like pathway is also required for the G2/M transition in vertebrate cells. Thus, NIMA may represent a new essential eukaryotic cell cycle regulator, although its homologues in other species are yet to be identified.
已证明CDC2可调控真核细胞进入有丝分裂。然而,在构巢曲霉中,如果另一种有丝分裂蛋白激酶NIMA未被激活,CDC2自身的激活并不足以触发有丝分裂。表面上看,NIMA和CDC2具有类似的功能,且调控方式相似。在细胞周期中,NIMA的活性受到严格调控。NIMA的过表达会诱导非洲爪蟾卵母细胞的生发泡破裂,并促进所有所检测的真核细胞过早进入有丝分裂,而显性负性突变体NIMA会在构巢曲霉和人类细胞中导致特异性的G2期阻滞,就如同CDC2的情况一样。然而,NIMA和CDC2具有截然不同的一级序列底物特异性。此外,控制细胞周期依赖性丰度、活性和定位的调控机制,对于NIMA而言很大程度上是分子内的,而对于CDC2则是分子间的。更重要的是,脊椎动物细胞的G2/M转换也需要一条类似NIMA的途径。因此,NIMA可能代表一种新的重要的真核细胞周期调节因子,尽管其在其他物种中的同源物尚未被鉴定出来。