Morris N R, James S W, O'Connell M J
Department of Pharmacology, University of Medicine and Dentistry of New Jersey, Robert W. Johnson Medical School, Piscataway 08854.
Ciba Found Symp. 1992;170:115-23; discussion 123-9. doi: 10.1002/9780470514320.ch8.
The nimA and bimE genes of Aspergillus nidulans respectively encode a 79 kDa protein kinase that is a positive regulator of mitosis and a 229 kDa protein that is a negative regulator of mitosis. Either overproduction of nimA or inactivation of bimE can induce mitosis and override the checkpoint associated with incomplete DNA replication. Double mutants between temperature-sensitive nimA and bimE alleles undergo chromatin condensation and spindle polymerization at restrictive temperature, suggesting that the p79nimA kinase is not required for chromatin condensation and spindle polymerization when bimE function is defective. In contrast double mutants carrying ts bimE and nimEcyclinB mutations or bimE and nimTcdc25 mutations are blocked in interphase at restrictive temperature. These results indicate that the mitotic block caused by inactivation of bimE requires activation of the p34cdc2/MPF kinase for chromatin condensation and spindle polymerization to occur. Antibodies against bimE fusion proteins have been used to study p229bimE in wild-type cells and cells overexpressing the bimE gene.
构巢曲霉的nimA和bimE基因分别编码一种79 kDa的蛋白激酶（它是有丝分裂的正调控因子）和一种229 kDa的蛋白（它是有丝分裂的负调控因子）。nimA的过量表达或bimE的失活均可诱导有丝分裂，并越过与不完全DNA复制相关的关卡。温度敏感型nimA和bimE等位基因之间的双突变体在限制温度下会发生染色质凝聚和纺锤体聚合，这表明当bimE功能有缺陷时，p79nimA激酶对于染色质凝聚和纺锤体聚合并非必需。相反，携带ts bimE和nimEcyclinB突变或bimE和nimTcdc25突变的双突变体在限制温度下会在间期被阻断。这些结果表明，由bimE失活导致的有丝分裂阻断需要p34cdc2/MPF激酶被激活，才能发生染色质凝聚和纺锤体聚合。针对bimE融合蛋白的抗体已被用于研究野生型细胞和过表达bimE基因的细胞中的p229bimE。
