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The role of plasma membrane H + ‐ ATP ase in jasmonate‐induced ion fluxes and stomatal closure in Arabidopsis thaliana
Author(s) -
Yan Suli,
McLamore Eric S.,
Dong Shanshan,
Gao Haibo,
Taguchi Masashige,
Wang Ningning,
Zhang Ting,
Su Xiaohua,
Shen Yingbai
Publication year - 2015
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.12915
Subject(s) - arabidopsis thaliana , arabidopsis , chemistry , methyl jasmonate , jasmonate , ion transporter , biophysics , plasma , closure (psychology) , microbiology and biotechnology , membrane , biochemistry , biology , gene , physics , mutant , quantum mechanics , economics , market economy
Summary Methyl jasmonate (Me JA ) elicits stomatal closure in many plant species. Stomatal closure is accompanied by large ion fluxes across the plasma membrane ( PM ). Here, we recorded the transmembrane ion fluxes of H + , Ca 2+ and K + in guard cells of wild‐type (Col‐0) Arabidopsis, the CORONATINE INSENSITIVE 1 ( COI 1 ) mutant coi1‐1 and the PM H + ‐ ATP ase mutants aha1‐6 and aha1‐7 , using a non‐invasive micro‐test technique. We showed that Me JA induced transmembrane H + efflux, Ca 2+ influx and K + efflux across the PM of Col‐0 guard cells. However, this ion transport was abolished in coi1‐1 guard cells, suggesting that Me JA ‐induced transmembrane ion flux requires COI 1. Furthermore, the H + efflux and Ca 2+ influx in Col‐0 guard cells was impaired by vanadate pre‐treatment or PM H + ‐ ATP ase mutation, suggesting that the rapid H + efflux mediated by PM H + ‐ ATP ases could function upstream of the Ca 2+ flux. After the rapid H + efflux, the Col‐0 guard cells had a longer oscillation period than before Me JA treatment, indicating that the activity of the PM H + ‐ ATP ase was reduced. Finally, the elevation of cytosolic Ca 2+ concentration and the depolarized PM drive the efflux of K + from the cell, resulting in loss of turgor and closure of the stomata.