Ataxia-telangiectasia mutated (ATM)-dependent activation of ATR occurs through phosphorylation of TopBP1 by ATM.

ATM (ataxia-telangiectasia mutated) is necessary for activation of Chk1 by ATR (ATM and Rad3-related) in response to double-stranded DNA breaks (DSBs) but not to DNA replication stress. TopBP1 has been identified as a direct activator of ATR. We show that ATM regulates Xenopus TopBP1 by phosphorylating Ser-1131 and thereby strongly ...
enhancing association of TopBP1 with ATR. Xenopus egg extracts containing a mutant of TopBP1 that cannot be phosphorylated on Ser-1131 are defective in the ATR-dependent phosphorylation of Chk1 in response to DSBs but not to DNA replication stress. Thus, TopBP1 is critical for the ATM-dependent activation of ATR following production of DSBs in the genome.
Mesh Terms:
Amino Acid Sequence, Animals, Ataxia Telangiectasia Mutated Proteins, Carrier Proteins, Cell Cycle Proteins, DNA Damage, DNA Repair, DNA-Binding Proteins, Enzyme Activation, Humans, Molecular Sequence Data, Oocytes, Phosphorylation, Protein-Serine-Threonine Kinases, Recombinant Proteins, Sequence Alignment, Serine, Tumor Suppressor Proteins, Xenopus Proteins, Xenopus laevis
J Biol Chem
Date: Jun. 15, 2007
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