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Publication : p38 and a p38-interacting protein are critical for downregulation of E-cadherin during mouse gastrulation.

First Author  Zohn IE Year  2006
Journal  Cell Volume  125
Issue  5 Pages  957-69
PubMed ID  16751104 Mgi Jnum  J:106348
Mgi Id  MGI:3618317 Doi  10.1016/j.cell.2006.03.048
Citation  Zohn IE, et al. (2006) p38 and a p38-interacting protein are critical for downregulation of E-cadherin during mouse gastrulation. Cell 125(5):957-69
abstractText  During vertebrate gastrulation, an epithelial to mesenchymal transition (EMT) is necessary for migration of mesoderm from the primitive streak. We demonstrate that p38 MAP kinase and a p38-interacting protein (p38IP) are critically required for downregulation of E-cadherin during gastrulation. In an ENU-mutagenesis screen we identified the droopy eye (drey) mutation, which affects splicing of p38IP. p38IP(drey) mutant embryos display incompletely penetrant defects in neural tube closure, eye development, and gastrulation. A stronger allele (p38IP(RRK)) exhibits gastrulation defects in which mesoderm migration is defective due to deficiency in E-cadherin protein downregulation in the primitive streak. We show that p38IP binds directly to p38 and is required for p38 activation in vivo. Moreover, both p38 and p38IP are required for E-cadherin downregulation during gastrulation. Finally, p38 regulates E-cadherin protein expression downstream from NCK-interacting kinase (NIK) and independently of the regulation of transcription by Fibroblast Growth Factor (Fgf) signaling and Snail.
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