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KAT5 tyrosine phosphorylation couples chromatin sensing to ATM signalling

Author

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  • Abderrahmane Kaidi

    (University of Cambridge)

  • Stephen P. Jackson

    (University of Cambridge
    The Wellcome Trust Sanger Institute)

Abstract

The detection of DNA lesions within chromatin represents a critical step in cellular responses to DNA damage. However, the regulatory mechanisms that couple chromatin sensing to DNA-damage signalling in mammalian cells are not well understood. Here we show that tyrosine phosphorylation of the protein acetyltransferase KAT5 (also known as TIP60) increases after DNA damage in a manner that promotes KAT5 binding to the histone mark H3K9me3. This triggers KAT5-mediated acetylation of the ATM kinase, promoting DNA-damage-checkpoint activation and cell survival. We also establish that chromatin alterations can themselves enhance KAT5 tyrosine phosphorylation and ATM-dependent signalling, and identify the proto-oncogene c-Abl as a mediator of this modification. These findings define KAT5 tyrosine phosphorylation as a key event in the sensing of genomic and chromatin perturbations, and highlight a key role for c-Abl in such processes.

Suggested Citation

  • Abderrahmane Kaidi & Stephen P. Jackson, 2013. "KAT5 tyrosine phosphorylation couples chromatin sensing to ATM signalling," Nature, Nature, vol. 498(7452), pages 70-74, June.
    • Handle: RePEc:nat:nature:v:498:y:2013:i:7452:d:10.1038_nature12201
    DOI: 10.1038/nature12201
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