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

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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)1,2. In Schizosaccharomyces pombe, mitotic checkpoints monitor DNA synthesis3 and the presence of DNA damage4,5. The replication-dependent mitotic checkpoint prevents mitosis by inactivating p34cdc2 kinase3. The mechanism by which the DNA damage checkpoint interacts with the mitotic machinery is distinct from that used by the replication checkpoint4,5. The activity of p34cdc2 is controlled, in part, by the wee1 protein kinase6, 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 report8 which suggested that the wee1 gene product was required for DNA damage-dependent mitotic arrest.