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lüll An imperfect G2M checkpoint contributes to chromosome instability following irradiation of S and G2 phase cells Krempler A; Deckbar D; Jeggo PA; Lobrich MCell Cycle 2007[Jul]; 6 (14): 1682-6DNA double strand break (DSB) repair and checkpoint control represent two major mechanisms that function to reduce chromosomal instability following ionizing irradiation (IR). Ataxia telangiectasia (A-T) cells have long been known to have defective checkpoint responses. Recent studies have shown that they also have a DSB repair defect following IR raising the issue of how ATM's repair and checkpoint functions interplay to maintain chromosomal stability. A-T and Artemis cells manifest an identical and epistatic repair defect throughout the cell cycle demonstrating that ATM's major repair defect following IR represents Artemis-dependent end-processing. Artemis cells show efficient G(2)/M checkpoint induction and a prolonged arrest relative to normal cells. Following irradiation of G(2) cells, this checkpoint is dependent on ATM and A-T cells fail to show checkpoint arrest. In contrast, cells irradiated during S phase initiate a G(2)/M checkpoint which is independent of ATM and, significantly, both Artemis and A-T cells show a prolonged arrest at the G(2)/M checkpoint likely reflecting their repair defect. Strikingly, the G(2)/M checkpoint is released before the completion of repair when approximately 10-20 DSBs remain both for S phase and G(2) phase irradiated cells. This defined sensitivity level of the G(2)/M checkpoint explains the prolonged arrest in repair-deficient relative to normal cells and provides a conceptual framework for the cooperative phenotype between checkpoint and repair functions in maintaining chromosomal stability.|*Chromosomal Instability[MESH]|Ataxia Telangiectasia Mutated Proteins[MESH]|Cell Cycle Proteins/genetics/metabolism[MESH]|Cell Division/*physiology[MESH]|DNA Damage[MESH]|DNA Repair[MESH]|DNA-Binding Proteins/genetics/metabolism[MESH]|DNA/genetics/metabolism/radiation effects[MESH]|Endonucleases[MESH]|G2 Phase/*physiology[MESH]|Humans[MESH]|Nuclear Proteins/genetics/metabolism[MESH]|Protein Serine-Threonine Kinases/genetics/metabolism[MESH]|Radiation, Ionizing[MESH]|S Phase/*physiology[MESH]|Tumor Suppressor Proteins/genetics/metabolism[MESH] |