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. 2015 Nov 13;12(2):357–368. doi: 10.1080/15548627.2015.1110667

Figure 2.

Figure 2.

Autophagy deficiency links TWIST1 to suppression of nucleotide excision repair. (A) Immunoblot analysis of XPC, TWIST1, SQSTM1 and GAPDH in WT and atg5 KO MEF cells lentivirally infected with shCon or 2 independent shRNAs targeting Twist1 (shTwist1 #1 or shTwist1 #2). (B) Immunoblot analysis of XPC, TWIST1, SQSTM1 and GAPDH in WT and sqstm1 KO MEF cells lentivirally infected with vector control (Con) or Myc-Twist1 expression vector. (C, D) Slot blot analysis of the levels of CPD (C) and 6-4PP (D) in WT and atg5 KO MEF cells lentivirally infected with shCon or shTwist1. Cells were collected for analysis at 0, 24 and 48 h post-UVB (10 mJ/cm2) for CPD and 0, 1 and 3 h post-UVB (10 mJ/cm2) for 6-4PP. (E, F) Quantification of percentage (%) of CPD repair (E) from C and 6-4PP repair (F) from D (mean±SD, n=3). *, P < 0.05, compared with WT group; #, P < 0.05, compared with KO+shCon group, Student t test. The results were obtained from 3 independent experiments.