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. 2011 Nov 2;108(46):18702–18707. doi: 10.1073/pnas.1109348108

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Fig. 5. — The insulin-signaling pathway regulates the stability of the adherens junction between ISCs and enteroblasts. (A) An FRT82B control ISC clone (green) 6 d ACI containing an ISC (arrowhead) and an enteroblast (arrow) adjacent (asterisk) to one another, as well as enterocytes. (B) A dInR³³⁹ mutant ISC clone (green) containing an ISC (arrowhead) and an enteroblast (arrow) in contact (asterisk). (C) A dInR³³⁹ mutant transit enteroblast clone (green, arrow) in contact (asterisk) with a wild-type intestinal stem cell (arrowhead). (A–C) Clone, GFP green; Delta, white vesicular; DE–cadherin, red; DAPI, blue nuclear. (Scale bar, 10 μm.) (D) DE–cadherin levels measured at the junction of the ISC and the enteroblast are significantly higher in dInR³³⁹ mutant clones than in FRT82B clones.