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Differential expression of receptors for Shiga and Cholera toxin is regulated by the cell cycle

Irina Majoul1, Tobias Schmidt, Maria Pomasanova

  • 1Max-Planck-Institute of Biophysical Chemistry, Department of Neurobiology, Göttingen, Germany. imajoul@gwdg.de

Journal of Cell Science
|February 28, 2002
PubMed

Insights

Cell cycle regulation controls toxin receptor expression. Cholera toxin binds in G0/G1, while Shiga toxin binds in G2/M, due to changes in glycolipid receptor synthesis.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Glycobiology

Background:

  • Cholera toxin and Shiga toxin bind to distinct glycolipid receptors, GM1 and Gb3, respectively, on cell surfaces.
  • Vero cells typically bind either Cholera toxin or Shiga toxin, but not both, suggesting differential receptor expression.

Purpose of the Study:

  • To investigate if cell cycle progression regulates the differential expression of Cholera toxin (GM1) and Shiga toxin (Gb3) receptors.
  • To understand the mechanism behind the cell-cycle-dependent regulation of these glycosphingolipid receptors.

Main Methods:

  • Utilizing synchronized and non-synchronized Vero cells to analyze toxin binding patterns across different cell cycle phases.
  • Quantifying the synthesis of specific glycolipid receptors (GM1 and Gb3) in relation to cell cycle stage.

Main Results:

  • Cholera toxin binding is preferential during the G0/G1 phases.
  • Shiga toxin binding is maximal during the G2 to telophase stages.
  • Differential receptor expression is attributed to cell-cycle-dependent synthesis of GM1 and Gb3, not transport or competition for precursors.

Conclusions:

  • Glycosphingolipid receptor expression is dynamically regulated by the cell cycle.
  • This cell-cycle-dependent regulation of toxin receptors is conserved across diverse cell types, including Vero cells, PC12 cells, and astrocytes.
  • The findings reveal a novel regulatory mechanism influencing cellular interactions with toxins.

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