Embryonic endocrine pancreas and mature β cells acquire α and PP cell phenotypes upon Arx misexpression
J. Clin. Invest. Patrick Collombat, et al. 117:961 doi:10.1172/JCI29115 [Go to this article.]

Figure 2
Conditional Arx misexpression restricted to the early pancreas results in a favoring of the glucagon- or PP-producing cell fates at the expense of the β and δ cell lineages. Sections of 6-week-old mice were examined for the presence of pancreatic hormones in cArxOE (A, D, G, J, M, and P), cArxOE::Pax6Cre (B, E, H, K, N, and Q), and cArxOE::Pdx1Cre (C, F, I, L, O, and R) animals by immunofluorescence. (A–C) The uniform GFP expression found in cArxOE mice (A) is expectedly excluded from the islets in cArxOE::Pax6Cre animals (B) and missing in cArxOE::Pdx1Cre pancreatic tissue (C). Conversely, the β-galactosidase activity is clearly detected in cArxOE::Pax6Cre islets (B, inset) and cArxOE::Pdx1Cre pancreata (C, inset). (D–R) The Cre-mediated misexpression of Arx in Pax6 or Pdx1 expression domains promotes a loss of β cell (D–F) and δ cell (G–I) populations, concurrently with an increase in numbers of glucagon-producing (D–O) or PP-producing (J–L) cell numbers. Arx production is uniformly detectable in the endocrine tissue of cArxOE::Pax6Cre and cArxOE::Pdx1Cre mice (M–O). Note that Arx is present in glucagon-labeled cells, and, most likely, in PP-positive cells (insets in N and O). A coexpression of Arx and PP was demonstrated both in controls (P) and in double-transgenic animals (Q and R). Each picture is representative of 6–15 independent animals. Glu, glucagon; Ins, insulin; Som, somatostatin. Original magnification, ×40.