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Overexpression of RelA causes G1 arrest and apoptosis in a pro-B cell line

A M Sheehy1, M S Schlissel

  • 1Graduate Program in Immunology, Departments of Medicine, Molecular Biology & Genetics, and Oncology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.

The Journal of Biological Chemistry
|March 20, 1999
PubMed

Insights

Elevated RelA levels induce cell cycle arrest and apoptosis in pro-B cells, but not mature B cells. This suggests NF-kappaB signaling plays a role in B cell development selection.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • NF-kappaB/Rel proteins are transcription factors regulating cellular responses like gene expression and apoptosis.
  • These proteins are post-translationally regulated and respond to extracellular stimuli.

Purpose of the Study:

  • To investigate the role of individual Rel family proteins in B cell development.
  • To determine the involvement of RelA and c-Rel in the signaling pathways of apoptosis.

Main Methods:

  • Overexpression of c-Rel or RelA using a tetracycline-regulated system in B cell lines (220-8, WEHI 231, M12).
  • Analysis of cell cycle progression and induction of apoptosis.

Main Results:

  • Overexpression of RelA, but not c-Rel, caused G1 cell cycle arrest and apoptosis in the pro-B cell line 220-8.
  • Both DNA binding and transactivation domains of RelA were essential for these effects.
  • RelA overexpression did not induce cell cycle arrest or apoptosis in immature (WEHI 231) or mature (M12) B cell lines.

Conclusions:

  • RelA-induced apoptosis is dependent on the B cell differentiation stage.
  • Differential sensitivity to NF-kappaB signaling may represent a selection mechanism during B cell development.

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