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Rbp‐j regulates expansion of pancreatic epithelial cells and their differentiation into exocrine cells during mouse development
Author(s) -
Fujikura Junji,
Hosoda Kiminori,
Kawaguchi Yoshiya,
Noguchi Michio,
Iwakura Hiroshi,
Odori Shinji,
Mori Eisaku,
Tomita Tsutomu,
Hirata Masakazu,
Ebihara Ken,
Masuzaki Hiroaki,
Fukuda Akihisa,
Furuyama Kenichiro,
Tanigaki Kenji,
Yabe Daisuke,
Nakao Kazuwa
Publication year - 2007
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.21310
Subject(s) - pdx1 , biology , pancreas , hes1 , endocrinology , medicine , enteroendocrine cell , endocrine system , cell growth , cellular differentiation , ductal cells , microbiology and biotechnology , epithelium , notch signaling pathway , signal transduction , gene , islet , insulin , genetics , hormone
Notch signaling regulates cell fate determination in various tissues. We have reported the generation of mice with a pancreas‐specific knockout of Rbp‐j using Pdx.cre mice. Those mice exhibited premature endocrine and ductal differentiation. We now generated mice in which the Rbp‐j gene was inactivated in Ptf1a‐expressing cells using Ptf1a.cre mice. The timing of the Cre‐mediated deletion in Rbp‐j f/f Ptf1a.cre mice is 1 day later than that in Rbp‐j f/f Pdx.cre mice. In Rbp‐j f/f Ptf1a.cre mouse pancreases, at E13.5, the reduced Hes1 expression was accompanied by reduced epithelial growth, but premature endocrine cell differentiation was minimal. At E15.5, Pdx1 expression was repressed and acinar cell differentiation was reduced, but an increase in acinar cell proliferation was observed during the perinatal period. Our study indicates that, in addition to its role in preventing premature differentiation of early endocrine cells, Rbp‐j regulates epithelial growth, Pdx1 expression, and acinar cell differentiation during mid‐pancreatic development. Developmental Dynamics 236:2779–2791, 2007. © 2007 Wiley‐Liss, Inc.