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裂殖酵母wee1蛋白激酶对于DNA损伤依赖性的有丝分裂停滞并非必需。

Fission yeast wee1 protein kinase is not required for DNA damage-dependent mitotic arrest.

作者信息

Barbet N C, Carr A M

机构信息

MRC Cell Mutation Unit, Sussex University, Falmer, UK.

出版信息

Nature. 1993 Aug 26;364(6440):824-7. doi: 10.1038/364824a0.

Abstract

Checkpoints maintain the dependency relationships between discrete events in the cell cycle (for example, ensuring mitosis does not occur before DNA replication is complete). In Schizosaccharomyces pombe, mitotic checkpoints monitor DNA synthesis and the presence of DNA damage. The replication-dependent mitotic checkpoint prevents mitosis by inactivating p34cdc2 kinase. The mechanism by which the DNA damage checkpoint interacts with the mitotic machinery is distinct from that used by the replication checkpoint. The activity of p34cdc2 is controlled, in part, by the wee1 protein kinase, which inactivates cdc2 through phosphorylation at tyrosine-15 (ref. 7). Here we report normal mitotic arrest after DNA damage in S. pombe cells in which the wee1 gene is defective or missing. We suggest why these findings contradict a recent report which suggested that the wee1 gene product was required for DNA damage-dependent mitotic arrest.

摘要

细胞周期中的关卡维持着离散事件之间的依赖关系(例如,确保在DNA复制完成之前不会发生有丝分裂)。在粟酒裂殖酵母中,有丝分裂关卡监测DNA合成以及DNA损伤的存在。依赖复制的有丝分裂关卡通过使p34cdc2激酶失活来阻止有丝分裂。DNA损伤关卡与有丝分裂机制相互作用的方式不同于复制关卡所使用的方式。p34cdc2的活性部分受wee1蛋白激酶控制,该激酶通过在酪氨酸-15位点磷酸化使cdc2失活(参考文献7)。在此,我们报道了在wee1基因有缺陷或缺失的粟酒裂殖酵母细胞中,DNA损伤后有丝分裂正常停滞。我们提出了为什么这些发现与最近一份报告相矛盾,该报告认为wee1基因产物是DNA损伤依赖性有丝分裂停滞所必需的。

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