Transcription profiling of mouse early endoderm from wild type and homeobox transcription factor Cdx2 knock-out strains

ABSTRACT: We demonstrate that conditional ablation of the homeobox transcription factor Cdx2 from early endoderm results in the replacement of the posterior intestinal epithelium with keratinocytes, a dramatic cell fate conversion caused by ectopic activation of the foregut/esophageal differentiation program. This anterior homeotic transformation is first evident in the early embryonic Cdx2-deficient gut as expression of several key foregut endoderm regulators was shifted caudally. While the intestinal transcriptome was severely affected, Cdx2-deficiency only transiently modified selected posterior Hox genes and the primary enteric Hox code was maintained. Further, we demonstrate that Cdx2-directed intestinal cell fate adoption plays an important role in the establishment of normal epithelial-mesenchymal interactions, as multiple signaling pathways involved in this process were severely affected. We conclude that Cdx2 controls important aspects of intestinal identity and development, and that this function is largely independent of the enteric Hox code. Gene ablation was achieved by creating a Cdx2 loxP/loxP mouse which was then crossed with a Foxa3-CRE mouse to yield Cdx2 loxP/loxP Foxa3-CRE mice.

ORGANISM(S): Mus musculus

SUBMITTER: Nan Gao 

PROVIDER: E-MTAB-92 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress