In the presence of DNA damage or incomplete DNA replication, eukaryotic cells activate cell cycle checkpoints that temporarily halt the cell cycle to permit DNA repair or completion of DNA replication to take place. In the presence of extensive damage or absence of timely repair, these checkpoint-signaling pathways may also trigger a pathway that effects programmed cell death or apoptosis (Ref.1). DNA damage-activated cell cycle checkpoints are regulated in part by the phosphoinositide kinase family of checkpoint components, including the yeast Rad3 in Schizosaccharomyces pombe, Mec1/Tel1 in Saccharomyces cerevisiae, mammalian ATM (Ataxia Telangiectasia-Mutated), ATR (ATM/Rad3-related), MEI-41 in Drosophila, and X-ATM and X-ATR in Xenopus. These checkpoint kinases regulate the activities of two downstream effector serine/threonine kinases, CDS1 and Chk1 (Csk [...]