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Multiple mechanisms regulate c-myc gene expression during normal T cell activation.

T Lindsten1, C H June, C B Thompson

  • 1Howard Hughes Medical Institute, University of Michigan, Ann Arbor 48109.

The EMBO Journal
|September 1, 1988
PubMed
Summary
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Normal human T cells regulate c-myc gene expression through multiple mechanisms. T cell receptor activation involves protein kinase C and calcium pathways, impacting transcriptional initiation and elongation for c-myc mRNA.

Area of Science:

  • Immunology
  • Molecular Biology
  • Gene Regulation

Background:

  • Quiescent T cells exhibit low c-myc mRNA due to limited promoter use, transcriptional blocks, and rapid mRNA degradation.
  • T cell activation via the T cell receptor (TCR)/CD3 complex upregulates c-myc mRNA expression.

Purpose of the Study:

  • To investigate the distinct intracellular pathways regulating c-myc gene expression during T cell activation.
  • To elucidate the roles of protein kinase C and intracellular calcium in c-myc transcriptional control.

Main Methods:

  • Stimulation of quiescent human T cells with phorbol myristate acetate (PMA) and ionomycin to mimic TCR signaling.
  • Analysis of c-myc mRNA levels and transcriptional regulation mechanisms (initiation and elongation).
  • Assessment of mRNA stability in the cytoplasm.

Related Experiment Videos

Main Results:

  • TCR/CD3 stimulation activates two complementary pathways: protein kinase C (PMA) and intracellular calcium (ionomycin).
  • Ionomycin enhances c-myc expression via increased transcriptional initiation.
  • PMA promotes c-myc expression partly by reducing transcriptional elongation blocks.
  • Both pathways' effects are enhanced by stabilizing c-myc mRNA.

Conclusions:

  • Multiple, cooperating mechanisms regulate c-myc gene expression during T cell activation.
  • Distinct signaling pathways differentially control transcriptional initiation and elongation.
  • Cytoplasmic mRNA stabilization further modulates c-myc expression levels.