Analysis of the sensing and transducing processes implicated in the stomatal responses to carbon dioxide in Commelina communis L.

It has been previously debated whether CO2 would depolarize the guard cell plasma membrane through malate-mediated activation of the anion channel. Moreover, it has been assessed that the CO2 signal would be transduced via cytosolic free Ca2+. In the present study, the CO2 sensing and transducing processes were reinvestigated in Commelina communis (L.) mainly by studying how L-(-)-malic acid and Ca2+ flux modulators affected different CO2 stomatal responses. L-(-)-malic acid (1 mM) inhibited by about 50% both CO2-induced stomatal closing and CO2-triggered inhibition of the stomatal opening response to the auxin indolyl-3-butyric acid. Stomatal dosing in response to atmospheric CO2 was strongly inhibited by the 1,4 dihydropyridines SDZ-202 791 R(-) (SDZ (-)) and nifedipine, and this inhibition was attenuated by the 1,4 dihydropyridines SDZ-202 791 S(+) and S-(-)-BAY K8644. Suboptimal concentrations of the slow anion channel blockers 5-nitro-2,3-phenylpropyllamine benzoic acid and anthracene-9-carboxylic acid increased the 50% inhibition of the CO2 closing response by the Ca2+ flux modulators SDZ (-) and 1,2-bis(o-aminophenoxy)ethane-N,N,N'N'-tetraacetic acid in a stronger manner than an additive one. Together, these results support the view that CO2 is sensed through reducing proton extrusion. Moreover, they might suggest that the CO2 signal is transduced through Ca2+ signalling arising from depolarization-mediated activation of a putative plasma membrane voltage-gated L-type Ca2+ channel and for which the plasma membrane slow anion channel is a potential target.