量研学術機関リポジトリ「QST-Repository」は、国立研究開発法人 量子科学技術研究開発機構に所属する職員等が生み出した学術成果（学会誌発表論文、学会発表、研究開発報告書、特許等）を集積しインターネット上で広く公開するサービスです。 Welcome to QST-Repository where we accumulates and discloses the academic research results(Journal Publications, Conference presentation, Research and Development Report, Patent, etc.) of the members of National Institutes for Quantum Science and Technology.
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The nuclear foci of phosphorylated histone H2AX (cH2AX) are frequently used as a marker for DNA double-strand breaks (DSBs) following ionizing radi- ation (IR). However, recent studies reported that cH2AX foci do not necessarily correlate with DSBs under other conditions. We showed that cH2AX foci induced by oxidative stress in hydrogen peroxide (H2O2)-treated cells displayed several different features from those induced by IR. The magnitude of cH2AX induction was heterogeneous among H2O2-treated cells. Some cells expressed small discrete cH2AX foci, whereas others expressed a gross cH2AX signal that was distributed throughout the nucleus. Oxidative stress-induced cH2AX was eliminated in DSB repair- deficient mutant cells as efficiently as in wild-type cells and was not necessarily accompanied by phosphorylated ataxia telangiectasia mutated (ATM) or 53BP1 foci. Analyses using specific inhibitors showed that ATM- and Rad3-related (ATR), rather than ATM, was the prominent kinase mediating the oxidative stress re- sponse. These results suggest that a major fraction of cH2AX induced by oxidative stress is not associated with DSBs. Single-stranded DNA arisen from stalled replication forks can cause the ATR-mediated induction of cH2AX. However, oxidative stress appeared to induce cH2AX in both S- and non-S-phase cells. These results suggest that there may be another path- way leading to the ATR-mediated induction of cH2AX in non-S-phase cells without DSBs.
Most hydrogen peroxide-induced histone H2AX phosphorylation is mediated by ATR and is not dependent on DNA double-strand breaks
