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.


Published in:
EMBO reports, 5, 3, 285-90
Year:
2004
ISSN:
1469-221X
Other identifiers:
Laboratories:


Note: The status of this file is: Involved Laboratories Only


 Record created 2009-04-02, last modified 2018-03-17

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