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A suppressor locus for MODY3-diabetes.

Miguel A Garcia-Gonzalez1,2,3, Claire Carette1,2,3, Alessia Bagattin1,2,3

  • 1Laboratoire d' Expression Génique, Développement et Maladies (EGDM), Département Développement, Reproduction et Cancer, INSERM U1016, Institut Cochin, Paris, France.

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|September 27, 2016
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Genetic backgrounds can suppress diabetes in Maturity Onset Diabetes of the Young type 3 (MODY3). A specific locus, Moda1, on mouse chromosome 3, was identified as a key genetic suppressor, restoring islet growth and function.

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Area of Science:

  • Genetics
  • Endocrinology
  • Molecular Biology

Background:

  • Maturity Onset Diabetes of the Young type 3 (MODY3), caused by HNF1A mutations, is a prevalent monogenic diabetes.
  • HNF1alpha deficiency impairs insulin secretion, but disease severity varies, suggesting modifier genes influence onset.
  • The precise molecular mechanisms underlying HNF1alpha-deficiency and diabetes variability remain unclear.

Purpose of the Study:

  • To investigate genetic modifiers that influence diabetes onset in HNF1alpha-deficient individuals.
  • To identify specific genetic loci that suppress diabetes in a mouse model of HNF1alpha-deficiency.
  • To elucidate the molecular mechanisms by which genetic background affects islet function in the absence of HNF1alpha.

Main Methods:

  • Utilized a mouse model for HNF1alpha-deficiency on different genetic backgrounds (C3H, CBA).
  • Performed genome scan analysis to identify diabetes suppressor loci.
  • Conducted comparative analysis of islet growth and function between diabetic-prone and resistant strains.

Main Results:

  • Identified a major diabetes suppressor locus, Moda1, on mouse chromosome 3 in resistant genetic backgrounds (C3H, CBA).
  • Moda1 contains 11 genes with non-synonymous SNPs interacting with loci on chromosomes 4, 11, and 18.
  • Absence of HNF1alpha caused postnatal defective islet growth in sensitive strains, which was restored in resistant strains.

Conclusions:

  • Specific genetic backgrounds possess powerful suppressors of diabetes in HNF1alpha-deficiency.
  • The Moda1 locus on mouse chromosome 3 plays a critical role in suppressing diabetes by restoring islet growth.
  • Findings are relevant to human genetics, as Moda1 is syntenic with a human locus associated with fasting glycemia.