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. Author manuscript; available in PMC: 2016 Sep 17.
Published in final edited form as: Mol Cell. 2015 Sep 10;59(6):1011–1024. doi: 10.1016/j.molcel.2015.07.029

Fig. 4. ATRi-treated cells recover via a Chk1-mediated mechanism.

Fig. 4

A. U2OS cells were treated with DMSO, ATRi (10 μM VE-821), or Chk1i (2 μM MK-8776). Levels of RPA32, pRPA32, and γH2AX were analyzed at the indicated times. B. U2OS cells were treated with increasing concentrations of ATRi or Chk1i for 24 h and then cultured in inhibitor-free media. Cell survival was analyzed 4 days after treatment. Error bar: S.D. (n=3). C. U2OS cells were treated with DMSO, ATRi, or Chk1i for 8 h. BrdU and γH2AX intensities were quantified in 1,200 cells at the indicated times. D. U2OS cells were treated with ATRi or Chk1i. Levels of chromatin-bound RPA were analyzed at the indicated times. E. U2OS cells were treated with ATRi, and levels of pChk1 and CDC25A were analyzed at the indicated times. F. Levels of CDC25A in U2OS cells treated with ATRi or Chk1i were compared at the indicated times. G. Amodel in which Chk1 promotes the recovery of ATRi-treated cells with moderate ssDNA. See also Fig. S4.