Expression data from E15.5 mouse embryos

The pancreatic beta cells are the only cells that can produce insulin in response to prevailing glycemia. The development of beta cells was found to be depending on the activity of a complex genetic network. Overexpression of transcriptional factor MafK in beta cells have resulted in impairment of thier functions and suppressed insulin secretion and increased the severity of beta cell loss resulting in an overt diabetes. We used microarrays to study the changes in islet gene expression profiles in MafK Tg. Mafk overexpression was expected to disrupt functions of genes containing MARE sites in their regulatory regions by bindig to cis-regulatory elements. Exploration of new factors with sunctional MAREs in thier regulatory regions in beta cells will improve our targeting stratigies for treatment of diabetes. A 0.78 kb full-length cDNA encoding the murine MafK protein including a FLAG peptide at the N-terminus was inserted into the rat insulin I promoter. Then, the construct was injected into BDF1-fertilized eggs to generate transgenic mice. All Tg mice were maintained on an ICR genetic background. Whole pancreata were collected from MafK transgenic embryos as well as wild type embryos at E15.5 (N=3 per each gentype). Total RNA was extracted and hybridized for Affymetrix microarray analysis.