Cyclic adenosine 5′‐diphosphoribose ( cADPR ) cyclic guanosine 3′,5′‐monophosphate positively function in Ca 2+ elevation in methyl jasmonate‐induced stomatal closure, cADPR is required for methyl jasmonate‐induced ROS accumulation NO production in guard cells

Methyl jasmonate ( M e JA ) signalling shares several signal components with abscisic acid ( ABA ) signalling in guard cells. Cyclic adenosine 5′‐diphosphoribose (c ADPR ) and cyclic guanosine 3′,5′‐monophosphate (c GMP ) are second messengers in ABA ‐induced stomatal closure. In order to clarify involvement of c ADPR and c GMP in M e JA ‐induced stomatal closure in Arabidopsis thaliana (Col‐0), we investigated effects of an inhibitor of c ADPR synthesis, nicotinamide ( NA ), and an inhibitor of c GMP synthesis, LY83583 (LY, 6‐anilino‐5,8‐quinolinedione), on M e JA ‐induced stomatal closure. Treatment with NA and LY inhibited M e JA ‐induced stomatal closure. NA inhibited M e JA ‐induced reactive oxygen species ( ROS ) accumulation and nitric oxide ( NO ) production in guard cells. NA and LY suppressed transient elevations elicited by M e JA in cytosolic free Ca 2+ concentration ([Ca 2+ ] cyt ) in guard cells. These results suggest that c ADPR and c GMP positively function in [Ca 2+ ] cyt elevation in M e JA ‐induced stomatal closure, are signalling components shared with ABA ‐induced stomatal closure in Arabidopsis , and that c ADPR is required for M e JA ‐induced ROS accumulation and NO production in Arabidopsis guard cells.