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Glucose‐ and mannose‐induced stomatal closure is mediated by ROS production, Ca 2+ and water channel in Vicia faba
Author(s) -
Li Yan,
Xu ShanShan,
Gao Jing,
Pan Sha,
Wang GenXuan
Publication year - 2016
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1111/ppl.12353
Subject(s) - salicylhydroxamic acid , chemistry , mannose , channel blocker , reactive oxygen species , catalase , biochemistry , egta , guard cell , vicia faba , antioxidant , biology , enzyme , botany , calcium , organic chemistry
Sugars act as vital signaling molecules that regulate plant growth, development and stress responses. However, the effects of sugars on stomatal movement have been unclear. In our study, we explored the effects of monosaccharides such as glucose and mannose on stomatal aperture. Here, we demonstrate that glucose and mannose trigger stomatal closure in a dose‐ and time‐dependent manner in epidermal peels of broad bean ( Vicia faba ). Pharmacological studies revealed that glucose‐ and mannose‐induced stomatal closure was almost completely inhibited by two reactive oxygen species ( ROS ) scavengers, catalase ( CAT ) and reduced glutathione ( GSH ), was significantly abolished by an NADPH oxidase inhibitor, diphenylene iodonium chloride ( DPI ), whereas they were hardly affected by a peroxidase inhibitor, salicylhydroxamic acid ( SHAM ). Furthermore, glucose‐ and mannose‐induced stomatal closure was strongly inhibited by a Ca 2+ channel blocker, LaCl 3 , a Ca 2+ chelator, ethyleneglycol‐bis(beta‐aminoethylether)‐N,N'‐tetraacetic acid ( EGTA ) and two water channel blockers, HgCl 2 and dimethyl sulfoxide ( DMSO ); whereas the inhibitory effects of the water channel blockers were essentially abolished by the reversing agent β‐mercaptoethanol (β‐ ME ). These results suggest that ROS production mainly via NADPH oxidases, Ca 2+ and water channels are involved in glucose‐ and mannose‐induced stomatal closure.