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Cell type-dependent control of NF-Y activity by TGF-beta

C Alabert1, L Rogers, L Kahn

  • 1Institut de Génétique Moléculaire de Montpellier, CNRS-UMR5535-IFR122, Montpellier, France.

Oncogene
|January 26, 2006
PubMed

Insights

Transforming growth factor beta (TGF-beta) activates the ERK cascade to move NF-YA into the nucleus, regulating gene expression. Cell type differences in MAPK pathway activation affect NF-YA

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Transforming growth factor beta (TGF-beta) is a cytokine regulating cell growth and differentiation.
  • TGF-beta signaling involves Smad pathways and MAPK cascades.
  • The transcription factor NF-Y plays a role in cellular processes.

Purpose of the Study:

  • To investigate the mechanism of TGF-beta-induced NF-Y activation.
  • To determine the role of MAPK pathways in TGF-beta-mediated NF-YA nuclear translocation.
  • To explore cell type-specific differences in TGF-beta signaling.

Main Methods:

  • Treatment of NIH3T3 fibroblasts and MDCK cells with TGF-beta.
  • Analysis of NF-YA nuclear translocation.
  • Assessment of MAPK pathway activation (ERK, p38).
  • Chromatin immunoprecipitation to measure NF-Y binding.

Main Results:

  • TGF-beta induces NF-YA nuclear translocation via ERK cascade activation.
  • NF-Y binding to chromatin and cyclin A2 gene transcription are increased by TGF-beta.
  • Cell type-specific differences in p38 and ERK activation kinetics were observed.
  • NIH3T3 fibroblasts showed delayed NF-YA nuclear accumulation compared to MDCK cells.

Conclusions:

  • TGF-beta1-induced NF-Y activation involves ERK1/2.
  • MAPK pathway interplay contributes to TGF-beta signaling.
  • Cell-specific kinetics of NF-YA relocalization suggest finely tuned transcriptional regulation.

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