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Reverse Yeast Two-hybrid System to Identify Mammalian Nuclear Receptor Residues that Interact with Ligands and/or Antagonists
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Reverse Yeast Two-hybrid System to Identify Mammalian Nuclear Receptor Residues that Interact with Ligands and/or Antagonists

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The nuclear hormone receptor coactivator NRC is a pleiotropic modulator affecting growth, development, apoptosis,

Muktar A Mahajan1, Sharmistha Das, Hong Zhu

  • 1Department of Pharmacology and Medicine, New York University School of Medicine, 550 First Ave., New York, NY 10016, USA.

Molecular and Cellular Biology
|May 15, 2004
PubMed

Insights

Nuclear hormone receptor coregulator (NRC) is vital for embryonic development, growth, and reproduction. NRC deficiency causes embryonic lethality and impaired wound healing, highlighting its crucial physiological roles.

Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Genetics

Background:

  • Nuclear hormone receptor coregulator (NRC) is a key protein interacting with nuclear hormone receptors and transcription factors.
  • Previous studies generated heterozygous NRC knockout mice (NRC+/-) on a mixed C57BL/6-129S6 background, which appeared normal.
  • Homozygous NRC deletion (NRC-/-) is embryonic lethal, indicating NRC's essential role in development.

Purpose of the Study:

  • To investigate the physiological functions of NRC.
  • To explore the impact of NRC deficiency on embryonic development, cell apoptosis, and reproductive capabilities.
  • To determine if strain background influences NRC knockout phenotypes.

Main Methods:

  • Generation of NRC+/- mice on C57BL/6-129S6 and 129S6 genetic backgrounds.
  • Analysis of embryonic lethality and developmental defects in NRC-/- embryos.
  • Derivation and analysis of mouse embryonic fibroblasts (MEFs) from NRC-/- embryos.
  • Assessment of fertility, growth, mortality, and wound healing in NRC+/- mice.

Main Results:

  • NRC-/- embryos exhibit growth retardation and die between 8.5 and 12.5 days postcoitus.
  • NRC-/- MEFs show increased apoptosis, and NRC knockdown in wild-type MEFs also enhances apoptosis.
  • 129S6 NRC+/- females display infertility (20%) or hypofertilety (80%), and males show reduced fertility.
  • 129S6 NRC+/- mice exhibit stunted growth, increased postnatal mortality, and impaired wound healing compared to controls.
  • Both C57/129 and 129S6 NRC+/- mice demonstrate spontaneous wound healing defects.

Conclusions:

  • NRC is essential for embryonic development, regulating growth and preventing apoptosis.
  • NRC plays a critical role in reproductive functions and postnatal survival.
  • NRC is indispensable for efficient wound repair.
  • NRC acts as a pleiotropic coregulator influencing diverse cellular and physiological processes.

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