Figure 1. OGG1 and MUTYH deficiency reduces sensitivity to acute oxidative telomere damage.

(A) Immunoblot of MUTYH and OGG1 in parental BJ FAP-TRF1 and MUTYH KO, OGG1 KO or DKO cell lines. α-tubulin and GAPDH used as loading controls.

(B) Immunoblot of TRF1 in parental and BJ FAP-TRF1 cell lines. β-actin used as a loading control.

(C) Cell counts of BJ FAP-TRF1 cell lines obtained 4 days after recovery from 20 min dye + light (DL) treatment, relative to untreated cells. Data are mean ± s.d. from 3 independent experiments; 2-way ANOVA; **p ≤ 0.01, ***p ≤ 0.001. ****p ≤ 0.0001.

(D) Representative images of β-galactosidase positive cells obtained 4 days after recovery from no treatment or 20 min DL treatment. Red arrows mark positive cells.

(E) Percent β-galactosidase positive cells. Data are mean ± s.d. from 4 independent experiments; 2-way ANOVA; **p ≤ 0.01; ***p ≤ 0.001; ****p ≤ 0.0001.

(F) Size of nuclear area (μm²) of cells obtained 4 days after recovery from no treatment or 20 min DL. Data are mean ± s.d. from total nuclei analyzed; each dot represents a nucleus; ordinary one-way ANOVA; comparisons *p ≤ 0.05; ****p ≤ 0.0001; comparison of untreated cell lines with untreated WT indicated by #p ≤ 0.05; ###p ≤ 0.001.