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An Efficient Method to Obtain Dedifferentiated Fat Cells
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The Polycomb-Dependent Epigenome Controls β Cell Dysfunction, Dedifferentiation, and Diabetes.

Tess Tsai-Hsiu Lu1, Steffen Heyne1, Erez Dror1

  • 1Max Planck Institute of Immunobiology and Epigenetics, Stuebeweg 51, 79108 Freiburg, Germany.

Cell Metabolism
|May 15, 2018
PubMed
Summary

Chromatin dysregulation, specifically Polycomb Repressive Complex 2 (PRC2) dysfunction, drives type 2 diabetes by causing beta cell dedifferentiation. This suggests a two-hit model involving both chromatin changes and hyperglycemia in diabetes progression.

Keywords:
EedPolycombcell identitychromatincomplex diseasesde-differentiationdiabetesepigenetictype 2 diabetesβ cells

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Area of Science:

  • Epigenetics and Molecular Biology
  • Endocrinology and Metabolism
  • Genomics and Computational Biology

Background:

  • The role of chromatin machinery in complex diseases like type 2 diabetes is not well understood.
  • Investigating epigenetic mechanisms offers potential insights into disease pathogenesis.

Purpose of the Study:

  • To investigate the contribution of chromatin dysregulation to type 2 diabetes (T2D) pathogenesis.
  • To identify specific epigenetic signatures associated with pancreatic beta cell dysfunction.

Main Methods:

  • Deep epigenome mapping and single-cell transcriptomics were employed to analyze chromatin states in T2D.
  • Functional studies involved assessing the impact of Polycomb Repressive Complex 2 (PRC2) loss of function in mouse models.

Main Results:

  • Two distinct chromatin-state signatures were identified, correlating with beta cell dysfunction in both mice and humans.
  • Ectopic activation of Polycomb-silenced domains and loss of lineage-defining genes were observed.
  • Loss of PRC2 in beta cells led to diabetes-mimicking transcriptional changes and beta cell dedifferentiation, independent of hyperglycemia.

Conclusions:

  • PRC2 is essential for maintaining pancreatic beta cell identity and function.
  • Chromatin dysregulation, particularly PRC2 dysfunction, is a significant contributor to T2D.
  • A two-hit model, involving both chromatin alterations and hyperglycemia, is proposed for beta cell failure in diabetes.