Multiple developmental defects derived from impaired recruitment of ASC-2 to nuclear receptors in mice: implication for posterior lenticonus with cataract

Mol Cell Biol. 2002 Dec;22(24):8409-14. doi: 10.1128/MCB.22.24.8409-8414.2002.

Abstract

ASC-2, a recently isolated transcriptional coactivator molecule, stimulates transactivation by multiple transcription factors, including nuclear receptors. We generated a potent dominant negative fragment of ASC-2, encompassing the N-terminal LXXLL motif that binds a broad range of nuclear receptors. This fragment, termed DN1, specifically inhibited endogenous ASC-2 from binding these receptors in vivo, whereas DN1/m, in which the LXXLL motif was mutated to LXXAA to abolish the receptor interactions, was inert. Interestingly, DN1 transgenic mice but not DN1/m transgenic mice exhibited severe microphthalmia and posterior lenticonus with cataract as well as a variety of pathophysiological phenotypes in many other organs. Our results provide a novel insight into the molecular and histopathological mechanism of posterior lenticonus with cataract and attest to the importance of ASC-2 as a pivotal transcriptional coactivator of nuclear receptors in vivo.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Motifs
  • Animals
  • Cells, Cultured
  • Congenital Abnormalities*
  • Disease Models, Animal
  • Embryo, Mammalian / anatomy & histology
  • Embryo, Mammalian / pathology
  • Embryo, Mammalian / physiology
  • Eye / pathology
  • Female
  • Fibroblasts / cytology
  • Fibroblasts / metabolism
  • Genes, Lethal
  • Genes, Reporter
  • Humans
  • Intracellular Signaling Peptides and Proteins*
  • Lens Diseases / genetics
  • Lens Diseases / metabolism*
  • Mice
  • Mice, Transgenic
  • Nuclear Receptor Coactivators
  • Peptide Fragments / genetics
  • Peptide Fragments / metabolism*
  • Phenotype
  • Pregnancy
  • Receptors, Cytoplasmic and Nuclear / metabolism*
  • Receptors, Retinoic Acid / metabolism
  • Signal Transduction / physiology
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*

Substances

  • Intracellular Signaling Peptides and Proteins
  • NCOA6 protein, human
  • Ncoa6 protein, mouse
  • Nuclear Receptor Coactivators
  • Peptide Fragments
  • Receptors, Cytoplasmic and Nuclear
  • Receptors, Retinoic Acid
  • Transcription Factors