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Related Experiment Videos

Oxidative signalling and gene expression during lymphocyte activation

S D Goldstone1, A D Milligan, N H Hunt

  • 1Department of Pathology, University of Sydney, Australia. goldston@icrf.icnet.uk

Biochimica Et Biophysica Acta
|November 8, 1996
PubMed
Summary

Reactive oxygen species (ROS) are crucial for T lymphocyte activation and cell cycle entry. This study identifies specific mRNAs regulated by ROS during the G0 to G1 phase transition in human cells.

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Intracellular reactive oxygen species (ROS) generation is essential for T lymphocyte activation.
  • ROS are proposed to act as signaling agents regulating cellular processes, including cell cycle entry.
  • The G0 to G1 phase transition requires both oxidative signaling and altered gene expression.

Purpose of the Study:

  • To determine which cell cycle entry events are affected by oxidative signaling.
  • To investigate the impact of oxidative signaling on global gene expression patterns during cell cycle entry.
  • To identify and characterize mRNAs responsive to oxidative signaling during this process.

Main Methods:

  • Differential display in a phenotypic screening approach to identify altered mRNA species.

Related Experiment Videos

  • Comparison of mRNA expression changes with cell cycle arrest induced by cyclosporin A.
  • RNAse protection assays to confirm redox regulation of specific mRNAs.

    • Main Results:

    • 10 mRNA species showed altered expression in response to inhibited oxidative signaling during cell cycle entry.
    • 4 of these mRNAs were unaffected by cyclosporin A-induced cell cycle arrest, indicating specific regulation.
    • RNAse protection assays confirmed redox regulation for 2 of these 4 mRNAs.

    Conclusions:

    • Oxidative signaling plays a significant role in regulating gene expression during the G0 to G1 phase transition.
    • Specific mRNAs are identified as being regulated by oxidative signaling, independent of general cell cycle arrest.
    • These findings suggest a critical role for ROS in the molecular mechanisms governing T cell cycle progression.