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Inhibition of nuclear receptor signalling by poly(ADP-ribose) polymerase

T Miyamoto1, T Kakizawa, K Hashizume

  • 1Department of Geriatrics, Endocrinology and Metabolism, Shinshu University School of Medicine, Matsumoto 390-8621, Japan. miyamoto@hsp.md.shinshu-u.ac.jp

Insights

Poly(ADP-ribose) polymerase (PARP) acts as a novel repressor of nuclear receptor signaling. Its enzymatic activity is crucial for inhibiting gene transcription mediated by nuclear receptors like retinoid X receptors (RXR).

Area of Science:

  • Molecular Biology
  • Gene Regulation
  • Cellular Signaling

Background:

  • Mammalian poly(ADP-ribose) polymerase (PARP) is a chromatin-associated protein involved in DNA repair and other nuclear processes.
  • Nuclear receptors, such as retinoid X receptors (RXR) and thyroid hormone receptors (TR), regulate gene expression in response to ligands.
  • The precise role of PARP in modulating nuclear receptor signaling pathways remained largely unexplored.

Purpose of the Study:

  • To investigate the potential role of PARP as a modulator of nuclear receptor signaling.
  • To determine if PARP directly interacts with nuclear receptors and affects their transcriptional activity.
  • To elucidate the mechanism by which PARP influences gene transcription regulated by nuclear receptors.

Main Methods:

  • Co-immunoprecipitation and gel shift assays to assess PARP binding to nuclear receptors (RXR and TR) and their DNA response elements.
  • Transient transfection experiments using wild-type and enzyme-defective PARP mutants to evaluate effects on nuclear receptor-mediated transcription.
  • Reporter gene assays with Gal4-fused PARP to determine its intrinsic transcriptional repressor activity.

Main Results:

  • PARP directly binds to retinoid X receptors (RXR), specifically within the DNA binding domain of RXRalpha.
  • PARP represses ligand-dependent transcriptional activity of TR-RXR heterodimers by binding to their response elements.
  • Enzymatically active PARP, but not an enzyme-defective mutant, significantly inhibited nuclear receptor function, indicating the importance of poly(ADP-ribosyl)ation.
  • PARP functions as a transcriptional repressor when recruited to a promoter, independent of its interaction with nuclear receptors.

Conclusions:

  • PARP acts as a novel negative cofactor in gene transcription, specifically modulating nuclear receptor superfamily signaling.
  • The poly(ADP-ribosyl)ation enzymatic activity of PARP is essential for its role in repressing nuclear receptor-mediated gene expression.
  • These findings reveal a new layer of regulation in nuclear receptor signaling, involving PARP-mediated transcriptional repression.

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