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. 2020 Mar 30;219(4):e201907213. doi: 10.1083/jcb.201907213

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© 2020 Subramanian et al.

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Figure 3. — Chemotherapy-induced DNA damage induces G2 arrest after a delay. (a and b) Representative images of γH2AX and DNA labeling (a) and quantification of γH2AX intensity (b) in Setx^+/+ (untreated), Setx^+/+ oocytes immediately after treatment with Eto (Eto-immediate), and Setx^−/−-ON oocytes. (c) Schematic depicting experimental models of “Eto-immediate” and “Eto-ON” oocytes. (d) GVBD rates for Eto-immediate and Eto-ON oocytes. (e) GVBD rates 5 and 20 h after release from IBMX for DMSO-treated control and Eto-ON oocytes. (f and g) Representative images of γH2AX and DNA labeling (f) and quantification of γH2AX intensity (g) in Eto-immediate and Eto-ON oocytes. Oocyte numbers are shown in parentheses from a minimum of three independent experiments. Error bars are mean ± SEM. Two-tailed Student’s t test (b, e, and g) or two-way ANOVA (d) was used for statistical analysis. ns, P > 0.05; *, P < 0.05; ***, P < 0.001; ****, P < 0.0001.

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