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DNA replication

The fragility of DNA

Nature Reviews Molecular Cell Biology volume 4, page 88 (2003)Cite this article

Reporting in Cell, Thomas Glover, graduate student Anne Casper and colleagues show that the replication checkpoint kinase ATR (ataxia-telangiectasia and Rad3-related) is a crucial factor in fragile-site stability. The authors were led to look at this kinase because ATR — along with the related ATM (ataxia-telangiectasia, mutated) — is implicated in the response to DNA damage during cellular replication.

To test the idea that ATM and ATR might be involved in fragile-site stability, Glover and co-workers first looked at the effects of 2-aminopurine (2-AP), which inhibits the kinase activities of both proteins. Although fragile-site gaps and breaks were seen when human lymphocytes were treated with aphidicolin alone, the addition of 2-AP led to a dramatic rise, with over 90% of these gaps occurring at known fragile sites.

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ORIGINAL RESEARCH PAPER

  1. Casper, A. M. et al. ATR regulates fragile site stability. Cell 111, 779–789 (2002)

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Authors
  1. Alison Mitchell
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Mitchell, A. The fragility of DNA. Nat Rev Mol Cell Biol 4, 88 (2003). https://doi.org/10.1038/nrm1034

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  • DOI: https://doi.org/10.1038/nrm1034

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