Labib K, Moreno S, Nurse P
ICRF Cell Cycle Laboratory, Department of Biochemistry, University of Oxford, UK.
J Cell Sci. 1995 Oct;108 ( Pt 10):3285-94. doi: 10.1242/jcs.108.10.3285.
The p34cdc2 kinase is essential for progression past Start in the G1 phase of the fission yeast cell cycle, and also acts in G2 to promote mitotic entry. Whilst very little is known about the G1 function of cdc2, the rum1 gene has recently been shown to encode an important regulator of Start in fission yeast, and a model for rum1 function suggests that it inhibits p34cdc2 activity. Here we present genetic data suggesting that rum1 maintains p34cdc2 in a pre-Start G1 form, inhibiting its activity until the cell achieves the critical mass required for Start, and find that in the absence of rum1 p34cdc2 has increased Start activity in vivo. It is also known that mutation of cdc2, or overexpression of rum1, can disrupt the dependency of S-phase upon mitosis, resulting in an extra round of S-phase in the absence of mitosis. We show that cdc2 and rum1 interact in this process, and describe dominant cdc2 mutants causing multiple rounds of S-phase in the absence of mitosis. We suggest that interaction of rum1 and cdc2 regulates Start, and this interaction is important for the regulation of S-phase within the cell cycle.
p34cdc2激酶对于裂殖酵母细胞周期G1期越过起始点进入下一阶段至关重要，并且在G2期也发挥作用以促进有丝分裂的启动。虽然对于cdc2在G1期的功能了解甚少，但最近研究表明rum1基因编码裂殖酵母中起始点的一个重要调节因子，关于rum1功能的一种模型认为它抑制p34cdc2的活性。在此我们提供遗传学数据表明rum1将p34cdc2维持在起始点前的G1期形式，抑制其活性直至细胞达到进入起始点所需的临界质量，并且发现在没有rum1的情况下，p34cdc2在体内具有增强的起始点活性。还已知cdc2的突变或rum1的过表达会破坏S期对有丝分裂的依赖性，导致在没有有丝分裂的情况下额外进行一轮S期。我们表明cdc2和rum1在此过程中相互作用，并描述了导致在没有有丝分裂的情况下出现多轮S期的显性cdc2突变体。我们认为rum1和cdc2的相互作用调节起始点，并且这种相互作用对于细胞周期内S期的调节很重要。
