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PRAMEL7 and CUL2 decrease NuRD stability to establish ground-state pluripotency.

Meneka Rupasinghe1,2, Cristiana Bersaglieri1, Deena M Leslie Pedrioli1

  • 1Department of Molecular Mechanisms of Disease, DMMD, University of Zurich, 8057, Zurich, Switzerland.

EMBO Reports
|February 8, 2024
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Summary
This summary is machine-generated.

PRAMEL7 reprograms advanced stem cells to a ground state by interacting with Cullin2 (CUL2). This interaction targets repressive chromatin regulators for degradation, restoring pluripotency gene expression.

Keywords:
Cullin 2Ground-state PluripotencyNuRDPRAMEL7UHRF1

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Area of Science:

  • Stem cell biology
  • Epigenetics
  • Molecular mechanisms of pluripotency

Background:

  • Pluripotency is established early in embryonic development.
  • Embryonic stem cells (ESCs) capture pluripotency but differ from the developmental ground state.
  • PRAMEL7 protein is key to achieving ground-state pluripotency.

Purpose of the Study:

  • To elucidate the mechanism by which PRAMEL7 reprograms gene expression.
  • To investigate the role of PRAMEL7-Cullin2 (CUL2) interaction in establishing ground-state pluripotency.

Main Methods:

  • Investigated PRAMEL7 association with Cullin2 (CUL2).
  • Assessed PRAMEL7-CUL2 complex recruitment to chromatin.
  • Analyzed proteasomal degradation of chromatin regulators, including the NuRD complex.

Main Results:

  • PRAMEL7 directly associates with CUL2, which is essential for ground-state gene expression.
  • The PRAMEL7-CUL2 complex targets NuRD for proteasomal degradation.
  • PRAMEL7 antagonizes NuRD-mediated repression, enhancing pluripotency gene expression via CUL2-dependent mechanisms.

Conclusions:

  • PRAMEL7-CUL2 interaction drives ground-state pluripotency by degrading NuRD.
  • This study links proteasomal degradation pathways to ground-state gene expression.
  • Findings offer insights for creating improved in vitro models of ground-state pluripotency.