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. 2011 Aug 12;6(8):e23432. doi: 10.1371/journal.pone.0023432

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Atsumi et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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A. DNA replication stress-associated tetraploidization was determined in MEFs (P4) with the formation of bi-nucleated tetraploidy (red arrowhead) after 0.2 mM HU treatment as illustrated (top-left panel). Tetraploidization was efficiently induced during primary growth but not in immortalized MEFs or p53-KO-MEFs. B. Repair efficiencies of DNA replication stress-associated lesions were compared between early passage (P2) and senescing MEFs (P6) after 48 h hydroxyurea (HU) treatment. γH2AX signal was used as a marker of DNA lesions, in which γH2AX signal and β-Actin signals in senescing MEFs (P6) were detected only with over-exposure compared to early passage MEFs (P2), due to decreased H2AX levels during senescence. The reduction in γH2AX signal after release was only evident in early passage MEFs, which suggests that senescing cells are defective in resolving DNA replication stress. C. A model of MEFs under serial cell proliferation either undergoing quiescence or developing immortality. While MEFs that maintain quiescence and diploidy show diminished H2AX levels, MEFs developing immortality accumulate γH2AX foci.