A Salt-Signaling Network Involving Ethylene, Extracellular ATP, Hydrogen Peroxide, and Calcium Mediates K + /Na + Homeostasis in Arabidopsis

This work aimed at investigating the interactive effects of salt-signaling molecules, i.e., ethylene, extracellular ATP (eATP), H O , and cytosolic Ca ([Ca ] ), on the regulation of K /Na homeostasis in . The presence of eATP shortened Col-0 hypocotyl length under no-salt conditions. Moreover, eATP...

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Veröffentlicht in:International journal of molecular sciences 2020-11, Vol.21 (22), p.8683
Hauptverfasser: Lang, Tao, Deng, Chen, Yao, Jun, Zhang, Huilong, Wang, Yin, Deng, Shurong
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Sprache:eng
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Zusammenfassung:This work aimed at investigating the interactive effects of salt-signaling molecules, i.e., ethylene, extracellular ATP (eATP), H O , and cytosolic Ca ([Ca ] ), on the regulation of K /Na homeostasis in . The presence of eATP shortened Col-0 hypocotyl length under no-salt conditions. Moreover, eATP decreased relative electrolyte leakage and lengthened root length significantly in salt-treated Col-0 plants but had no obvious effects on the ethylene-insensitive mutants and . Steady-state ionic flux kinetics showed that exogenous 1-aminocyclopropane-1-carboxylic acid (ACC, an ethylene precursor) and eATP-Na (an eATP donor) significantly increased Na extrusion and suppressed K loss during short-term NaCl treatment. Moreover, ACC remarkably raised the fluorescence intensity of salt-elicited H O and cytosolic Ca . Our qPCR data revealed that during 12 h of NaCl stress, application of ACC increased the expression of and , which encode the plasma membrane (PM) Na /H antiporters (SOS1) and H -ATPase (H pumps), respectively. In addition, eATP markedly increased the transcription of , , and , and ACC treatment of Col-0 roots under NaCl stress conditions caused upregulation of and /3, which directly contribute to the H O and Ca signaling pathways, respectively. Briefly, ethylene was triggered by eATP, a novel upstream signaling component, which then activated and strengthened the H O and Ca signaling pathways to maintain K /Na homeostasis under salinity.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms21228683