Abstract
Pasteurella multocida toxin (PMT) is a highly potent mitogen for a variety of cell types. PMT has been shown to induce various cellular signaling processes, and it has been suggested to function through the heterotrimeric G-proteins G(q)/G(11). To analyze the role of G(q)/G(11) in the action of PMT, we have studied the effect of the toxin in Galpha(q)/Galpha(11) double-deficient fibroblasts as well as in fibroblasts lacking only Galpha(q) or Galpha(11). Interestingly, formation of inositol phosphates in response to PMT was exclusively dependent on Galpha(q) but not on the closely related Galpha(11). Although Galpha(q)/Galpha(11) double-deficient and Galpha(q)-deficient cells did not respond with any production of inositol phosphates to PMT, PMT was still able to induce various other cellular effects in these cells, including the activation of Rho, the Rho-dependent formation of actin stress fibers and focal adhesions, as well as the stimulation of c-Jun N-terminal kinase and extracellular signal-regulated kinase. These data show that PMT leads to a variety of cellular effects that are mediated only in part by the heterotrimeric G-protein G(q).
Highlights
Pasteurella multocida toxin (PMT) is a highly potent mitogen for a variety of cell types
For studies on the possible role of Gq/G11 in the cellular effects of PMT, we employed fibroblast cell lines derived from mouse embryos deficient in either G␣q or G␣11 or lacking both G-protein ␣-subunits
Even at PMT concentrations that were maximally effective in wild-type fibroblasts, no effect on inositol phosphate levels could be observed in G␣q/G␣11 double-deficient fibroblasts (Fig. 2B)
Summary
Pasteurella multocida toxin (PMT) is a highly potent mitogen for a variety of cell types. G␣q/G␣11 double-deficient and G␣q-deficient cells did not respond with any production of inositol phosphates to PMT, PMT was still able to induce various other cellular effects in these cells, including the activation of Rho, the Rho-dependent formation of actin stress fibers and focal adhesions, as well as the stimulation of c-Jun N-terminal kinase and extracellular signal-regulated kinase.
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