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Am J Physiol Gastrointest Liver Physiol 286: G872-G880, 2004. First published January 8, 2004; doi:10.1152/ajpgi.00326.2003
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HORMONES AND SIGNALING

Putative intestine-specific enhancers located in 5' sequence of the CDX1 gene regulate CDX1 expression in the intestine

Erinn B. Rankin,* Wei Xu,* Debra G. Silberg, and EunRan Suh

Gastroenterology Division, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104

Submitted 31 July 2003 ; accepted in final form 31 December 2003

CDX1 is a homeobox transcription factor that plays a critical role in intestinal epithelial cell growth and differentiation. CDX1 gene expression is tightly regulated in a temporal and cell-type specific manner. However, very little is known about the regulatory mechanisms that direct CDX1 gene expression in the intestine. To elucidate these mechanisms, we employed a series of transgenic mouse studies using the 5' flanking sequences of the human CDX1 gene. Transgenic mice containing nucleotides between -5667 and +68 relative to the transcription start site of the CDX1 gene demonstrated ectopic expression of the transgene in the brain and gastric smooth muscle. However, transgenic expression of the nucleotides -15601 to +68 of the CDX1 gene was restricted to the intestinal epithelium, which was identical to endogenous CDX1 gene expression. Taken together, the upstream sequences between -15601 and -5667 contain regulatory elements that direct transgene expression specifically to the intestinal epithelium. Furthermore, DNase I hypersensitivity assays revealed two active chromatin regions in the CDX1 gene (hypertensive sites 1 and 2) located at approximately -5.8 and -6.8 kb upstream of the CDX1 gene, respectively, which may function as potential intestine-specific enhancers.

transgenic mice; homeobox protein


Address for reprint requests and other correspondence: E. Suh, Gastroenterology Div., Dept. of Medicine, Univ. of Pennsylvania, Ste. 600, 415 Curie Blvd., Philadelphia, PA 19104 (E-mail: suher{at}mail.med.upenn.edu).






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