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Analysis of the sensing and transducing processes implicated in the stomatal responses to carbon dioxide in Commelina communis L.
Author(s) -
Cousson A.
Publication year - 2000
Publication title -
plant, cell and environment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.646
H-Index - 200
eISSN - 1365-3040
pISSN - 0140-7791
DOI - 10.1046/j.1365-3040.2000.00561.x
Subject(s) - guard cell , chemistry , depolarization , bay k8644 , biophysics , channel blocker , membrane potential , biochemistry , calcium , receptor , biology , agonist , organic chemistry
It has been previously debated whether CO 2 would depolarize the guard cell plasma membrane through malate‐mediated activation of the anion channel. Moreover, it has been assessed that the CO 2 signal would be transduced via cytosolic free Ca 2 + . In the present study, the CO 2 sensing and transducing processes were reinvestigated in Commelina communis (L.) mainly by studying how L ‐(–)‐malic acid and Ca 2 + flux modulators affected different CO 2 stomatal responses. L ‐(–)‐malic acid (1 m M ) inhibited by about 50% both CO 2 ‐induced stomatal closing and CO 2 ‐triggered inhibition of the stomatal opening response to the auxin indolyl‐3‐butyric acid. Stomatal closing in response to atmospheric CO 2 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 CO 2 closing response by the Ca 2 + 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 CO 2 is sensed through reducing proton extrusion. Moreover, they might suggest that the CO 2 signal is transduced through Ca 2 + signalling arising from depolarization‐mediated activation of a putative plasma membrane voltage‐gated L‐type Ca 2 + channel and for which the plasma membrane slow anion channel is a potential target.