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 |
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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. |
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ISSN: | 1422-0067 1661-6596 1422-0067 |
DOI: | 10.3390/ijms21228683 |