Tyrosine dephosphorylation of H2AX modulates apoptosis and survival decisions

Peter J. Cook, Bong Gun Ju, Francesca Telese, Xiangting Wang, Christopher K. Glass and Michael G. Rosenfeld ()
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Peter J. Cook: Howard Hughes Medical Institute School of Medicine, University of California, San Diego, California 92037, USA
Bong Gun Ju: Howard Hughes Medical Institute School of Medicine, University of California, San Diego, California 92037, USA
Francesca Telese: Howard Hughes Medical Institute School of Medicine, University of California, San Diego, California 92037, USA
Xiangting Wang: Howard Hughes Medical Institute School of Medicine, University of California, San Diego, California 92037, USA
Christopher K. Glass: School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA
Michael G. Rosenfeld: Howard Hughes Medical Institute School of Medicine, University of California, San Diego, California 92037, USA

Nature, 2009, vol. 458, issue 7238, 591-596

Abstract: Abstract Life and death fate decisions allow cells to avoid massive apoptotic death in response to genotoxic stress. Although the regulatory mechanisms and signalling pathways controlling DNA repair and apoptosis are well characterized, the precise molecular strategies that determine the ultimate choice of DNA repair and survival or apoptotic cell death remain incompletely understood. Here we report that a protein tyrosine phosphatase, EYA, is involved in promoting efficient DNA repair rather than apoptosis in response to genotoxic stress in mammalian embryonic kidney cells by executing a damage-signal-dependent dephosphorylation of an H2AX carboxy-terminal tyrosine phosphate (Y142). This post-translational modification determines the relative recruitment of either DNA repair or pro-apoptotic factors to the tail of serine phosphorylated histone H2AX (γ-H2AX) and allows it to function as an active determinant of repair/survival versus apoptotic responses to DNA damage, revealing an additional phosphorylation-dependent mechanism that modulates survival/apoptotic decisions during mammalian organogenesis.

Date: 2009
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DOI: 10.1038/nature07849

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