Differential expression of receptors for Shiga and Cholera toxin is regulated by the cell cycle.
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.
Majoul
Irina
I
Max-Planck-Institute of Biophysical Chemistry, Department of Neurobiology, Göttingen, Germany. imajoul@gwdg.de
Schmidt
Tobias
T
Pomasanova
Maria
M
Boutkevich
Evgenia
E
Kozlov
Yuri
Y
Söling
Hans-Dieter
HD
D000818:Animals; D002453:Cell Cycle; D002478:Cells, Cultured; D002522:Chlorocebus aethiops; D005677:G(M1) Ganglioside / Q000096:biosynthesis / Q000378:metabolism*; D016193:G1 Phase; D016195:G2 Phase; D006624:Hippocampus / Q000166:cytology; D051379:Mice; D009474:Neurons / Q000378:metabolism; D016716:PC12 Cells; D051381:Rats; D011956:Receptors, Cell Surface / Q000096:biosynthesis / Q000378:metabolism*; D016192:Resting Phase, Cell Cycle; D013692:Telophase; D014281:Trihexosylceramides / Q000096:biosynthesis / Q000378:metabolism*; D014709:Vero Cells
D011956:Receptors, Cell Surface; D014281:Trihexosylceramides; C023552:choleragen receptor; D005677:G(M1) Ganglioside; C018549:globotriaosylceramide