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Ligand-dependent contribution of RXRbeta to cholesterol homeostasis in Sertoli cells.

We show that mice expressing retinoid X receptor beta (RXRbeta) impaired in its transcriptional activation function AF-2 (Rxrb(af20) mutation) do not display the spermatid release defects observed in RXRbeta-null mutants, indicating that the role of RXRbeta in spermatid release is ligand-independent. In contrast, like RXRbeta-null mutants, Rxrb(af20) mice accumulate cholesteryl esters in Sertoli cells (SCs) due to reduced ABCA1 transporter-mediated cholesterol efflux. We provide genetic and molecular evidence that cholesterol homeostasis in SCs does not require PPARalpha and beta, but depends upon the TIF2 coactivator and RXRbeta/LXRbeta heterodimers, in which RXRbeta AF-2 is transcriptionally active. Our results also indicate that RXRbeta may be activated by a ligand distinct from 9-cis retinoic acid.

Pubmed ID: 14993927


  • Mascrez B
  • Ghyselinck NB
  • Watanabe M
  • Annicotte JS
  • Chambon P
  • Auwerx J
  • Mark M


EMBO reports

Publication Data

March 2, 2004

Associated Grants

  • Agency: NIDDK NIH HHS, Id: 1-P01-DK59820-01

Mesh Terms

  • ATP-Binding Cassette Transporters
  • Animals
  • Cholesterol
  • DNA-Binding Proteins
  • Dimerization
  • Electrophoretic Mobility Shift Assay
  • Gene Expression Regulation
  • Gene Silencing
  • Histone Acetyltransferases
  • Homeostasis
  • Immunochemistry
  • Ligands
  • Male
  • Mice
  • Mice, Knockout
  • Nuclear Receptor Coactivator 1
  • Nuclear Receptor Coactivator 2
  • Orphan Nuclear Receptors
  • Protein Binding
  • Receptors, Cytoplasmic and Nuclear
  • Retinoid X Receptor beta
  • Sertoli Cells
  • Spermatids
  • Transcription Factors