Reexpression of retinoic acid receptor (RAR)γ or overexpression of RARα or RARβ in RARγ-null F9 cells reveals a partial functional redundancy between the three RAR types Academic Article Article uri icon

Overview

MeSH Major

  • Autophagy
  • Leukemia, Promyelocytic, Acute
  • Receptors, Retinoic Acid

abstract

  • Disruption of retinoic acid receptor (RAR) gamma in F9 embryonal carcinoma cells leads to aberrent differentiation and reduced activation of expression of several all-trans-retinoic acid (RA)-induced genes. We have analyzed the expression of several additional RA-responsive genes in RAR alpha- and RAR gamma-null F9 cells. The RA-induced activation of Cdx1, Gap43, Stra4, and Stra6 was specifically impaired in RAR gamma-null cells, supporting the idea that each RAR may regulate distinct subsets of target genes. To further investigate the role of RAR gamma in F9 cell differentiation, "rescue" cell lines reexpressing RAR gamma 2 or overexpressing either RAR alpha 1 or RAR beta 2 were established in RAR gamma-null cells. Reexpression of RAR gamma or overexpression of RAR alpha restored both target-gene activation and the differentiation potential. In contrast, over-expression of RAR beta only poorly restored differentiation, although it could replace RAR gamma for the activation of target genes. Functional redundancy between the various RARs is discussed.

publication date

  • August 15, 1995

Research

keywords

  • Academic Article

Identity

Digital Object Identifier (DOI)

  • 10.1073/pnas.92.17.7854

PubMed ID

  • 7644503

Additional Document Info

start page

  • 7854

end page

  • 8

volume

  • 92

number

  • 17