Cdx2 Initiates Histodifferentiation of the Midgut Endoderm

FEBS Lett. 2008 Jul 23;582(17):2555-60. doi: 10.1016/j.febslet.2008.06.024. Epub 2008 Jun 23.

Abstract

Null mutation or haploinsufficiency of Cdx2 results in the development of heterotopic lesions with a gastric phenotype in the midgut endoderm. Conversely transgenic expression of Cdx2 in the stomach causes the endoderm to differentiate into intestinal-type mucosa. We demonstrate that the mesoderm adjacent to intestinal heterotopic areas expresses stomach specific Barx1 while the surrounding mesoderm is Barx1 negative. We conclude that the initiation of gut histodifferentiation lies in the endodermal expression of Cdx2 and that endodermal/mesodermal cross-talk involving Barx1 with appropriate feedback loops results in the development of the postnatal gut phenotype.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CDX2 Transcription Factor
  • DNA-Binding Proteins / metabolism
  • Embryo, Mammalian / metabolism
  • Endoderm / metabolism*
  • Female
  • Gastric Mucosa / metabolism
  • HMGB Proteins / metabolism
  • Homeodomain Proteins / genetics
  • Homeodomain Proteins / metabolism*
  • Intestinal Mucosa / metabolism
  • Intestines / embryology*
  • Male
  • Mesoderm / metabolism
  • Mice
  • Mice, Mutant Strains
  • Mice, Transgenic
  • Morphogenesis* / genetics
  • SOXB1 Transcription Factors
  • Stomach / embryology*
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*

Substances

  • Barx1 protein, mouse
  • CDX2 Transcription Factor
  • Cdx2 protein, mouse
  • DNA-Binding Proteins
  • HMGB Proteins
  • Homeodomain Proteins
  • SOXB1 Transcription Factors
  • Sox2 protein, mouse
  • Transcription Factors