Figure 7: BPTF is dispensable for pancreatic differentiation but its inactivation delays the onset and progression of c-MYC-driven pancreatic tumors.

(a) PCR on genomic DNA showing efficient recombination at the Bptf locus in Bptf^P−/− pancreas (top). RT–qPCR analysis of BPTF WT and mutant mRNA species in control (n=6) and Bptf^P−/− (n=7) mice (bottom). Transcript levels were normalized against actin and the WT condition. (b) Haematoxylin–eosin staining of WT and Bptf^P−/− mouse pancreatic sections. D, duct; V, blood vessel; *, islet of langerhans. Scale bar, 200 μm. (c) mRNA expression of acinar transcription factors, digestive enzymes and endocrine markers in pancreata of WT and Bptf^P−/− mice assessed by RT–qPCR (n=3 per genotype). Transcript levels were normalized against actin and the WT condition. (d) PCR on pancreas (P) genomic DNA assessing the extent of recombination at the Bptf locus in 5–7-week-old Ptf1a-CreERT2^+/KI;Ela-Myc mice of the corresponding genotypes. Liver (L) samples were used as negative controls. (e) Kaplan–Meier curves of tumour-free survival are shown for Ela-Myc mice of the indicated Bptf genotypes. *P<0.05 (log-rank test). (f) Tumour volume of Ela-Myc mice of the indicated Bptf genotypes as determined by ultrasound. Data are expressed as the mean±s.e.m. ****P<0.00001 (Wilcoxon test). (g) PCR analysis of genomic DNA from tumours arising in Bptf^P+/+, Bptf^P−/+ and Bptf^P−/−; Ela-Myc mice.