Rad2p-induced cell growth arrest is released by rad9 deletion but is not affected by downstream DNA damage checkpoint genes

초록

Mitotic catastrophe, a failure of mitosis, arouses endopolyploidy, giant cell formation, and eventually delayed cell death. Mitotic catastrophe is induced by defective cell cycle checkpoints and by DNA damages such as some anticancer drugs and ionizing radiation, and microtubuledestabilizing agents. RAD2 is a yeast endonuclease in nucleotide excision repair. Here we show that Rad2p overexpression alone, in the absence of extrinsic DNA dan\mage, causes cell growth arrest and mitotic catastrophe. Interestingly, the Rad2p-induced cell growth arrest is not caused by the catalytic activity of Rad2p, but rather by its C-terminal region. Cells growth-arrested by Rad2p induction do not show apoptotic phenotypes and YCA1, a yeast caspase homolog, deltion does not affect cell growth arrest by Rad2p induction. However, Rad2p-induced cell growth arrest is released by rad9 deletion but is not affected by downstream DNA damage checkpoint genes. These observations suggest that RAD2 ha a function in coordinating cell cycle regulation and damaged DNA repair.