4.4 Article

Inactivation of Fgfr2 gene in mouse secondary palate mesenchymal cells leads to cleft palate

Journal

REPRODUCTIVE TOXICOLOGY
Volume 77, Issue -, Pages 137-142

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.reprotox.2018.03.004

Keywords

Secondary palate; Fgfr2; Palate initiation; Cleft palate

Funding

  1. National Institutes of Health, USA (COBRE program of the National Center for Research Resources) [P20RR017702, DE016845]
  2. Kentucky Science and Engineering Foundation [KSEF-2070-RDE-013]

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Numerous studies have been conducted to understand the molecular mechanisms controlling mammalian secondary palate development such as growth, reorientation and fusion. However, little is known about the signaling factors regulating palate initiation. Mouse fibroblast growth factor (FGF) receptor 2 gene (Fgfr2) is expressed on E11.5 in the palate outgrowth within the maxillary process, in a region that is responsible for palate cell specification and shelf initiation. Fgfr2 continues to express in palate on E12.5 and E13.5 in both epithelial and mesenchymal cells, and inactivation of Fgfr2 expression in mesenchymal cells using floxed Fgfr2 allele and Osr2-Cre leads to cleft palate at various stages including reorientation, horizontal growth and fusion. Notably, some mutant embryos displayed no sign of palate shelf formation suggesting that FGF receptor 2 mediated FGF signaling may play an important role in palate initiation. (C) 2018 Published by Elsevier Inc.

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