Pharmacological evidence for the implication of both cyclic GMP-dependent and -independent transduction pathways within auxin-induced stomatal opening in Commelina communis (L.).

It has been previously suggested that auxin-induced stomatal opening results from at least two transduction pathways, one of which involves cyclic GMP (cGMP) as the mediator within a Ca(2+) signalling cascade. This hypothesis was investigated further in epidermal peels of Commelina communis by comparing the effects of potential inhibitors of plant Ca(2+)-dependent enzymes on the stomatal opening responses to the auxin indolyl-3-butyric acid (IBA) and to the cGMP membrane-permeable derivative 8-bromoguanosine 3',5'-cyclic monophosphate (8-Br-cGMP). In the 30-50 &mgr;M range, the potential plant calmodulin (CaM) antagonist N-(aminohexyl)-5-chloro-1-naphthalenesulphonamide (W-7) positively interacted with IBA but not with 8-Br-cGMP to open the stomata. The CaM antagonists W-7 (in the 10-20 &mgr;M range) and N-(aminohexyl)-1-naphthalenesulphonamide (40 &mgr;M), the potential inhibitors of plant protein kinases 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (20 and 200 &mgr;M) and K-252a (0.6 &mgr;M), and cyclosporine A and FK506, potential inhibitors of plant homologs of Ca(2+)-CaM complex (Ca(2+)/CaM)-dependent protein phosphatase 2B, prevented the IBA and 8-Br-cGMP responses by about 70% and 100%, respectively. Together, these results provide indirect pharmacological evidence that, in addition to the cGMP-dependent pathway, the auxin signal is transduced through at least one cGMP-independent pathway.