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

¹ Max-Planck-Institute of Biophysical Chemistry, Department of Neurobiology, Göttingen, Germany
² Engelhardt Institute of Molecular Biology, Department of Molecular Biology, Vavilova Street 32, Moscow, Russia and The Oslo University Center for Medical Studies at Moscow, Vasilova Street 34/5, Moscow, Russia
³ Medical Institute, Minsk, Belorussia

^* Authors for correspondence (e-mail: imajoul{at}gwdg.de ; hsoelin{at}gwdg.de )

Accepted 5 November 2001

Cholera and Shiga toxin bind to the cell surface via glycolipid receptors GM1 and Gb3, respectively. Surprisingly, the majority of Vero cells from a non-synchronized population bind either Cholera or Shiga toxin but not both toxins. The hypothesis that the differential expression of toxin receptors is regulated by the cell cycle was tested. We find that Cholera toxin binds preferentially in G0/G1, with little binding through S-phase to telophase, whereas Shiga toxin binds maximally through G2 to telophase but does not bind during G0/G1 and S-phase. The changes result from the corresponding changes in Gb3 and GM1 synthesis, not from variations of receptor transport to the cell surface. The changes do not reflect competition of Gb3 and GM1 synthesis for lactosylceramide. Cells as diverse as Vero cells, PC12 cells and astrocytes show the same cell-cycle-dependent regulation of glycosphingolipid receptors, suggesting that this novel phenomenon is based on a conserved regulatory mechanism.

Key words: AB5-toxins, Glycosphingolipid receptors, Cell cycle, Golgi

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