Figure 2
Figure 2. Quiescent B lymphocytes are deficient in global genome repair. (A) Time-course of repair of UV-induced lesions in quiescent and proliferating B lymphocytes and in WT and XP-E B lymphoblasts after exposure to 5 J/m2 UV light. DNA samples, 1 μg for (6-4)PPs and 60 ng for CPDs, were blotted in triplicate on nitrocellulose membranes, and the amount of lesions was visualized with anti-CPDs and anti-(6-4)PPs antibodies. (B) Quantification of at least 3 experiments, including the aforementioned one, with ImageGauge software. To control for variations in DNA load, blots were reprobed with a 32P-labeled genomic probe, and the antibody signal was normalized against genomic DNA. Data are shown as mean ± SEM. The difference in repair efficiencies between quiescent and proliferating B lymphocytes was statistically significant as determined by paired Student t test, P < .05, n = 30 donors. (C) Repair of CPDs and (6-4)PPs lesions in quiescent (top) and proliferating B lymphocytes (bottom) at 24 hours after exposure to various doses of UV. Data are representative of 2 experiments and are shown as mean ± SEM. The difference in repair efficiencies between quiescent and proliferating B lymphocytes was statistically significant as determined by paired Student t test, P < .05, n = 6 donors.

Quiescent B lymphocytes are deficient in global genome repair. (A) Time-course of repair of UV-induced lesions in quiescent and proliferating B lymphocytes and in WT and XP-E B lymphoblasts after exposure to 5 J/m2 UV light. DNA samples, 1 μg for (6-4)PPs and 60 ng for CPDs, were blotted in triplicate on nitrocellulose membranes, and the amount of lesions was visualized with anti-CPDs and anti-(6-4)PPs antibodies. (B) Quantification of at least 3 experiments, including the aforementioned one, with ImageGauge software. To control for variations in DNA load, blots were reprobed with a 32P-labeled genomic probe, and the antibody signal was normalized against genomic DNA. Data are shown as mean ± SEM. The difference in repair efficiencies between quiescent and proliferating B lymphocytes was statistically significant as determined by paired Student t test, P < .05, n = 30 donors. (C) Repair of CPDs and (6-4)PPs lesions in quiescent (top) and proliferating B lymphocytes (bottom) at 24 hours after exposure to various doses of UV. Data are representative of 2 experiments and are shown as mean ± SEM. The difference in repair efficiencies between quiescent and proliferating B lymphocytes was statistically significant as determined by paired Student t test, P < .05, n = 6 donors.

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