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. Author manuscript; available in PMC: 2014 Oct 1.
Published in final edited form as: Transgenic Res. 2013 Mar 15;22(5):965–972. doi: 10.1007/s11248-013-9700-0

Fig. 4. Nkx2.2flox/flox;Pdx1-cre mutants recapitulate the Nkx2.2 null pancreatic phenotype.

Fig. 4

Using immunofluorescent staining for the expression of glucagon, the presence of alpha cells was observed in the pancreas from Nkx2.2flox/+ (a) and Nkx2.2flox/flox (b) embryos at E15.5, whereas a significant decrease of alpha cells was observed in the Nkx2.2flox/flox;Pdx1-cre pancreas (c). The known pattern of expression for Nkx2.2 was observed in the control pancreas sections (d, e) compared with the efficient loss of Nkx2.2 in the mutant (f) due to Pdx1-cre mediated recombination of the Nkx2.2flox allele. Similar to the phenotype observed in the Nkx2.2 null mice, pups were born and had severely elevated blood glucose (g). DAPI marks nuclei (a–c). Images are 20X