Salicylic acid improves salinity tolerance in Arabidopsis by restoring membrane potential and preventing salt-induced K+ loss via a GORK channel

Despite numerous reports implicating salicylic acid (SA) in plant salinity responses, the specific ionic mechanisms of SA-mediated adaptation to salt stress remain elusive. To address this issue, a non-invasive microelectrode ion flux estimation technique was used to study kinetics of NaCl-induced n...

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Veröffentlicht in:Journal of experimental botany. - 1985. - 64(2013), 8 vom: 10. Mai, Seite 2255-68
1. Verfasser: Jayakannan, Maheswari (VerfasserIn)
Weitere Verfasser: Bose, Jayakumar, Babourina, Olga, Rengel, Zed, Shabala, Sergey
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2013
Zugriff auf das übergeordnete Werk:Journal of experimental botany
Schlagworte:Journal Article Research Support, Non-U.S. Gov't H+ flux H+-ATPase K+ flux depolarization membrane potential outward-rectifying K+ channel potassium homeostasis. Plant Growth Regulators mehr... Potassium Channels Sodium Chloride 451W47IQ8X Salicylic Acid O414PZ4LPZ Potassium RWP5GA015D
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245 1 0 |a Salicylic acid improves salinity tolerance in Arabidopsis by restoring membrane potential and preventing salt-induced K+ loss via a GORK channel 
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520 |a Despite numerous reports implicating salicylic acid (SA) in plant salinity responses, the specific ionic mechanisms of SA-mediated adaptation to salt stress remain elusive. To address this issue, a non-invasive microelectrode ion flux estimation technique was used to study kinetics of NaCl-induced net ion fluxes in Arabidopsis thaliana in response to various SA concentrations and incubation times. NaCl-induced K(+) efflux and H(+) influx from the mature root zone were both significantly decreased in roots pretreated with 10-500 μM SA, with strongest effect being observed in the 10-50 μM SA range. Considering temporal dynamics (0-8-h SA pretreatment), the 1-h pretreatment was most effective in enhancing K(+) retention in the cytosol. The pharmacological, membrane potential, and shoot K(+) and Na(+) accumulation data were all consistent with the model in which the SA pretreatment enhanced activity of H(+)-ATPase, decreased NaCl-induced membrane depolarization, and minimized NaCl-induced K(+) leakage from the cell within the first hour of salt stress. In long-term treatments, SA increased shoot K(+) and decreased shoot Na(+) accumulation. The short-term NaCl-induced K(+) efflux was smallest in the gork1-1 mutant, followed by the rbohD mutant, and was highest in the wild type. Most significantly, the SA pretreatment decreased the NaCl-induced K(+) efflux from rbohD and the wild type to the level of gork1-1, whereas no effect was observed in gork1-1. These data provide the first direct evidence that the SA pretreatment ameliorates salinity stress by counteracting NaCl-induced membrane depolarization and by decreasing K(+) efflux via GORK channels 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 4 |a H+ flux 
650 4 |a H+-ATPase 
650 4 |a K+ flux 
650 4 |a depolarization 
650 4 |a membrane potential 
650 4 |a outward-rectifying K+ channel 
650 4 |a potassium homeostasis. 
650 7 |a Plant Growth Regulators  |2 NLM 
650 7 |a Potassium Channels  |2 NLM 
650 7 |a Sodium Chloride  |2 NLM 
650 7 |a 451W47IQ8X  |2 NLM 
650 7 |a Salicylic Acid  |2 NLM 
650 7 |a O414PZ4LPZ  |2 NLM 
650 7 |a Potassium  |2 NLM 
650 7 |a RWP5GA015D  |2 NLM 
700 1 |a Bose, Jayakumar  |e verfasserin  |4 aut 
700 1 |a Babourina, Olga  |e verfasserin  |4 aut 
700 1 |a Rengel, Zed  |e verfasserin  |4 aut 
700 1 |a Shabala, Sergey  |e verfasserin  |4 aut 
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