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. 2010 Jun 7;107(25):11537–11542. doi: 10.1073/pnas.1001261107

Fig. 2.

Fig. 2.

DNA damage repair, cell death, and division after low-dose infection with pks+ E. coli. CHO cells were infected for 4 h with live pks+ or pks E. coli with an MOI of 5–20 bacteria per cell or were left uninfected (Ctrl). At the end of the infection, the cells were washed and grown with gentamicin. (A) Cell-cycle analysis 16 and 30 h after infection. (B) γH2AX levels were quantified by flow cytometry 16 or 30 h after infection. (C) CHO or xrs-6 Ku80-defective cells were infected; 24 h later, apoptotic cells were labeled with a carboxyfluorescein fluoromethyl ketone peptide inhibitor of caspases (FLICA) for 1 h and quantified by flow cytometry. Error bars represent SE from three experiments. (D) The cells were examined by confocal microscopy for DNA (blue), Ser10-phosphorylated histone H3 (pH3, red), and γH2AX (green) 24 h after infection. (Scale bars, 10 μm.) (E) Quantification of γH2AX foci in mitotic cells. Error bars represent SEs from three experiments.