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Significance Recently, the potassium voltage-gated channel, KQT-like subfamily Q, member1 (KCNQ1 ) gene has received much attention as a candidate susceptibility gene for type 2 diabetes in Asian, European, and other populations. The molecular mechanism underlying the association ofKCNQ1 with the onset of type 2 diabetes has remained unclear; however, we have now found that a paternal allelic mutation ofKcnq1 results in the up-regulation of the neighboring imprinted gene cyclin-dependent kinase inhibitor 1C (Cdkn1c ), a cell cycle inhibitor, in pancreatic β-cells of mice, with this effect being mediated by epigenetic modification of theCdkn1c promoter. These changes seem to be responsible for the reduced pancreatic β-cell mass and impaired glucose tolerance characteristics ofKcnq1 mutant mice.

Paternal allelic mutation at the Kcnq1 locus reduces pancreatic β-cell mass by epigenetic modification of Cdkn1c