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ATM and ATR are two related kinases essential for signalling DNA damage. Although ATM is thought to be the principle kinase responsible for signalling ionising radiation (IR)-induced DNA damage, ATR also contributes to signalling this form of genotoxic stress. However, the molecular basis of differential ATM and ATR activation in response to IR remains unclear. Here, we report that ATR is recruited to sites of IR-induced DNA damage significantly later than activation of ATM. We show that ATR is recruited to IR-induced nuclear foci in G(1) and S phase of the cell cycle, supporting a role for ATR in detecting DNA damage outside of S phase. In addition, we report that recruitment of ATR to sites of IR-induced DNA damage is concomitant with appearance of large tracts of single-stranded DNA (ssDNA) and that this event is dependent on ATM and components of the Mre11/Rad50/Nbs1 (MRN) protein complex.

Original publication

DOI

10.1038/sj.onc.1209426

Type

Journal article

Journal

Oncogene

Publication Date

29/06/2006

Volume

25

Pages

3894 - 3904

Keywords

3T3 Cells, Animals, Ataxia Telangiectasia Mutated Proteins, Base Sequence, Cell Cycle Proteins, DNA Damage, DNA Repair Enzymes, DNA, Single-Stranded, DNA-Binding Proteins, HeLa Cells, Humans, Mice, Protein-Serine-Threonine Kinases, RNA, Small Interfering, Radiation, Ionizing, S Phase, Tumor Suppressor Proteins