It has been suggested that the intestinal endoderm is responsive to signals received\ud from underlying mesoderm, indicating cross-talk between the layers. Cdx2 mutant\ud mice develop heterotopias of stomach-type epithelium within the paracaecal region of\ud the intestine. They are therefore an ideal in-vivo model in which to study whether the\ud loss of endodermal gene expression required for intestinal development leads to\ud stomach-specific mesodermal gene expression.\ud In this study, Sox2, a stomach endoderm-specific marker, was used to detect gastric\ud heterotopias in Cdx2 mutant embryonic intestine using whole-mount in-situ\ud hybridisation. The nature of the underlying mesoderm was investigated using a\ud second marker, Barx1, which is known to be specifically expressed in the stomach\ud mesoderm. RT-PCR was used to detect low levels of Barx1 expression in Cdx2+/-\ud caecum samples. Further investigation using in-situ hybridisation techniques\ud indicated regions of Barx1 expression in a similar distribution to the regions detected\ud using the Sox2 probe. This finding confirms that the mesoderm underlying the Cdx2\ud mutant gastric heterotopias expresses a stomach-specific gene and therefore that\ud the mesoderm is responsive to endodermal signals.\ud It has been suggested that Cdx2+/- mice do not develop gastric-type intestinal\ud heterotopias postnatally. If proven, this would indicate that intestinal stem cell\ud potential becomes limited at some point during development and prevents the\ud epithelium responding to a postnatal loss of Cdx2 protein. A conditional Cdx2 mouse\ud model is required in order to investigate this hypothesis. The creation of this mouse\ud model formed the second part of this project. Following creation of a targeting vector,\ud transfection into ES cells and injection into blastocysts, chimeric mice were obtained.\ud These mice were successfully bred for germline transmission
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