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The Men1 gene has been identified as the gene responsible for MEN-1, a hereditary syndrome transmitted as an autosomal dominant trait. Disruption of the Men1 gene results in defects in the development of multiple organs, including pancreatic islets. Homozygous disruption of Men1 in mice causes embryonic lethality, making it difficult to determine the genes involved in defects of pancreatic islets during embryonic development. In this study, embryoid bodies formed from null mutant (Men1-/-) and wild-type (Men1+/+) embryonic stem cells were used as a model system to investigate the effects of the Men1 gene on pancreatic islet development. Using RT-PCR, SOX17, FOXA2 and NKX2.2 were found to be differentially expressed between the two embryoid bodies. Additionally, the gene expression profile of these Men1-/- embryoid bodies was characterized in detail by DNA microarray techniques, and a series of putative menin-targeted genes was identified. Our study suggests a critical role for Men1 in pancreatic islet development, and indicates that genes such as SOX17, FOXA2, NKX2.2 and SOX4 are potential targets of Men1.

Differentially expressed genes in Men1 knockout and wild‑type embryoid bodies for pancreatic islet development