Fig. 5: Rad51b mutant MEFs show an increased susceptibility to MMC-induced DNA damage. | Cell Death & Differentiation

Fig. 5: Rad51b mutant MEFs show an increased susceptibility to MMC-induced DNA damage.

From: A truncating variant of RAD51B associated with primary ovarian insufficiency provides insights into its meiotic and somatic functions

Fig. 5

A Cell proliferation assay of WT and mutant Rad51b primary MEFs at passage 2 (p + 2) incubated in presence of a continuous treatment with MMC. The results are expressed as a percentage relative to the control (not treated with MMC). Each point on the graph represents the mean ± SD. B Percentage of colonies obtained by clonogenic cell survival assays after treatment with MMC. The results are expressed as a percentage relative to the control (untreated) of Rad51bWT/WT and Rad51bKI/KI immortalized cells. C Representative γH2AX immunolabelling of WT and mutant Rad51b at 72 h. Quantification of γH2AX foci in Rad51b WT and mutant MEFs. Rad51bWT/WT and Rad51bKI/KI MEFs at p + 2 were incubated in presence of MMC at 1 µg/ml for 1 h and then supplemented with fresh medium without MMC. The quantification was performed at different time points: 0 h: 0 h, 6 h: 6 h, 24 h: 24 h, 48 h; 48 h and 72 h: 72 h. Cells were classified in 5 groups: 0 foci, 1 to 10 foci, 10 to 30 foci, 30 to 150 foci and >150 foci. n = 3. Rad51bc.92delT/c.92delT variant is referred as Rad51bKI/KI for simplicity. Welch´s t-test analysis: *p < 0.05; **p < 0.01. Bar in panel, 10 µm.

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