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. Author manuscript; available in PMC: 2015 Jun 26.
Published in final edited form as: Cell Rep. 2014 Jun 5;7(6):1849–1857. doi: 10.1016/j.celrep.2014.04.029

Fig. 3. The A-G-20 and C-E-F modules exhibit non-redundant functions in the chromatin recruitment of the FA core complex and resistance to crosslink damage.

Fig. 3

(A) Immunoblot detecting monoubiquitination of FANCD2 and chromatin-bound FANCL in cells exposed to mitomycin C (left panel) or cisplatin (right panel) in wild-type HCT116 (WT) and the indicated knockout/knockdown mutant cells. See also Fig. S4.

(B) Quantification of chromatin-bound FANCL (left panel of A) in wild-type HCT116 (WT), FANCG−/− + Ctrl shRNA, WT + shFANCF alone (shFANCF), FANCG−/− + shFANCF, and FANCL−/− cells exposed to mitomycin C. See also Fig. S4.

(C) Clonogenic survival of parental HCT116 (WT), FANCG−/− + Ctrl shRNA, FANCG−/− + shFANCF, and FANCL−/− cells treated with mitomycin C. See also Fig. S4.

(D) Clonogenic survival of parental DT40 (WT), FANCE−/−, FANCG−, and FANCE−/− FANCG− cells treated with cisplatin. See also Fig. S2C.

Error bars for chromatin-bound FANCL quantification (B) and clonogenic survivals (C and D) were derived from SDs from three or more independent tests.