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PPM1A Controls Diabetic Gene Programming through Directly Dephosphorylating PPARγ at Ser273.

Keon Woo Khim1, Sun Sil Choi1, Hyun-Jun Jang1

  • 1Department of Biological Sciences, Ulsan National Institute of Science and Technology (UNIST), Ulsan 44919, Korea.

Cells
|February 7, 2020
PubMed
Summary

Protein phosphatase PPM1A dephosphorylates PPARγ at Ser273, restoring diabetic gene expression. PPM1A levels decrease in obesity models, suggesting PPM1A as a therapeutic target for metabolic disorders.

Keywords:
PPARγ S273 phosphorylationPPM1Adiabetic gene reprogramminginsulin sensitivityobesity

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Area of Science:

  • Molecular Biology
  • Metabolic Disease Research
  • Signal Transduction

Background:

  • Peroxisome proliferator-activated receptor γ (PPARγ) regulates adipose tissue and is implicated in obesity-linked metabolic disorders.
  • Phosphorylation of PPARγ at Ser273 by CDK5/ERK dysregulates gene expression, contributing to diabetic conditions.
  • The mechanisms of PPARγ dephosphorylation at Ser273 are not well understood, limiting therapeutic development.

Purpose of the Study:

  • To identify and characterize novel phosphatases involved in PPARγ dephosphorylation at Ser273.
  • To investigate the role of identified phosphatases in the context of insulin resistance and obesity.
  • To explore the therapeutic potential of targeting PPARγ dephosphorylation for metabolic disorders.

Main Methods:

  • Biochemical assays to identify PPARγ phosphatase activity.
  • In vitro and in vivo studies to validate the function of identified phosphatases.
  • Analysis of gene expression using microarray and GTEx data.
  • Studies in diet-induced obese (DIO) and db/db mouse models of insulin resistance.

Main Results:

  • Protein phosphatase Mg2+/Mn2+-dependent 1A (PPM1A) was identified as a novel PPARγ phosphatase that directly dephosphorylates Ser273.
  • PPM1A dephosphorylation of PPARγ restores dysregulated diabetic gene expression.
  • PPM1A expression is significantly decreased in DIO and db/db mice, correlating negatively with pSer273.
  • Human transcriptomic data show positive correlations between PPM1A and genes dysregulated by pSer273.

Conclusions:

  • PPM1A directly dephosphorylates PPARγ at Ser273, counteracting the effects of aberrant phosphorylation in metabolic disease.
  • Decreased PPM1A expression in insulin resistance models highlights its role in disease pathogenesis.
  • PPM1A represents a promising therapeutic target for treating obesity-linked metabolic disorders.