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. 2011 Jan 31;286(13):11427–11433. doi: 10.1074/jbc.M110.188797

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© 2011 by The American Society for Biochemistry and Molecular Biology, Inc.

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FIGURE 2. — Requirement for Math1 in secretory cell metaplasia induced by loss of Notch activity. A, Alcian blue-positive goblet cells increased substantially after tamoxifen treatment of RBP-Jκ^Fl/Fl;Villin-Cre^(ER-T2) mice but not of Math1^Fl/Fl;Villin-Cre^(ER-T2) (top) or RBP-Jκ^Fl/Fl;Math1^Fl/Fl;Villin-Cre^(ER-T2) (bottom) mice. Similarly, Math1^Fl/Fl;Villin-Cre^(ER-T2), and RBP-Jκ^Fl/Fl;Math1^Fl/Fl;Villin-Cre^(ER-T2) small intestines lacked all Crs4c1-expressing Paneth and ChromograninA (ChgA)-positive EE cells, indicating loss of all secretory lineages with lone loss of Math1 or combined absence of Math1 and RBP-Jκ. Failure of secretory cell metaplasia was equally evident in the duodenum (top rows) and ileum (bottom rows). B, expression of intestinal alkaline phosphatase (AP) and the microvillus brush border marker phospho-Ezrin/Radixin/Moesin (p-ERM) was notably reduced in RBP-Jκ^Fl/Fl;Villin-Cre^(ER-T2) mice after tamoxifen treatment, reflecting significant enterocyte loss, but restored in RBP-Jκ^Fl/Fl;Math1^Fl/Fl;Villin-Cre^(ER-T2) mice and preserved in Math1^Fl/Fl;Villin-Cre^(ER-T2) mice. The results indicate that Notch signaling is dispensable for enterocyte maturation, at least when Math1 is absent. Scale bars = 50 μm.