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TAK1 activation of the mouse JunB promoter is mediated through a CCAAT box and NF-Y

B J Eggen1, G F Benus, S Folkertsma

  • 1Developmental Genetics, Groningen Biomolecular Sciences and Biotechnology Institute, University of Groningen, Kerklaan 30, 9751 NN, Haren, The Netherlands. b.j.l.eggen@biol.rug.nl

FEBS Letters
|October 17, 2001
PubMed

Insights

Transforming growth factor beta activated kinase 1 (TAK1) activates the JunB gene. This activation is mediated by the nuclear factor Y (NF-Y) transcription factor binding to a CCAAT motif in the JunB promoter.

Area of Science:

  • Molecular Biology
  • Gene Regulation
  • Signal Transduction

Background:

  • JunB gene expression is regulated by various stimuli, including transforming growth factor beta (TGFbeta) and interleukin-6 (IL-6).
  • TGFbeta activated kinase 1 (TAK1) is a key kinase involved in TGFbeta, bone morphogenetic protein (BMP), and interleukin-1 (IL-1) signaling pathways.

Purpose of the Study:

  • To investigate the mechanism by which TAK1 influences JunB gene promoter activity.
  • To identify specific DNA elements and transcription factors involved in TAK1-mediated JunB activation.

Main Methods:

  • JunB promoter analysis to identify regulatory elements.
  • Reporter gene assays to measure promoter activity.
  • Site-directed mutagenesis to assess the role of the CCAAT motif.
  • Expression of dominant-negative constructs to inhibit transcription factor function.

Main Results:

  • A CCAAT motif within the JunB gene promoter was identified as essential for TAK1-mediated activation.
  • Transferring this CCAAT element to a minimal promoter conferred TAK1 responsiveness.
  • The CCAAT-binding transcription factor, nuclear factor Y (NF-Y), was found to activate the JunB promoter.
  • A dominant-negative NF-YA construct inhibited TAK1-induced JunB activation.

Conclusions:

  • TAK1-mediated activation of the JunB gene is dependent on the CCAAT-binding transcription factor NF-Y.
  • NF-Y binding to the CCAAT motif in the JunB promoter is a critical step in this signaling pathway.

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