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- Title
A Critical Role of Sodium Flux via the Plasma Membrane Na<sup>+</sup>/H<sup>+</sup> Exchanger SOS1 in the Salt Tolerance of Rice.
- Authors
El Mahi, Houda; Pérez-Hormaeche, Javier; De Luca, Anna; Villaltac, Irene; Espartero, Joaquín; Gámez-Arjona, Francisco; Fernández, José Luis; Bundó, Mireia; Mendoza, Imelda; Mieulet, Delphine; Lalanne, Eric; Sang-Yeol Lee; Dae-Jin Yun; Guiderdoni, Emmanuel; Aguilar, Manuel; Leidi, Eduardo O.; Pardo, José M.; Quintero, Francisco J.
- Abstract
Rice (Oryza sativa) stands among the world's most important crop species. Rice is salt sensitive, and the undue accumulation of sodium ions (Na+) in shoots has the strongest negative correlation with rice productivity under long-term salinity. The plasma membrane Na+/H+ exchanger protein Salt Overly Sensitive 1 (SOS1) is the sole Na+ efflux transporter that has been genetically characterized to date. Here, the importance of SOS1-facilitated Na+ flux in the salt tolerance of rice was analyzed in a reverse-genetics approach. A sos1 loss-of-function mutant displayed exceptional salt sensitivity that was correlated with excessive Na+ intake and impaired Na+ loading into the xylem, thus indicating that SOS1 controls net root Na+ uptake and long-distance Na+ transport to shoots. The acute Na+ sensitivity of sos1 plants at low NaCl concentrations allowed analysis of the transcriptional response to sodicity stress without effects of the osmotic stress intrinsic to high-salinity treatments. In contrast with that in the wild type, sos1 mutant roots displayed preferential down-regulation of stress-related genes in response to salt treatment, despite the greater intensity of stress experienced by the mutant. These results suggest there is impaired stress detection or an inability to mount a comprehensive response to salinity in sos1. In summary, the plasma membrane Na+/H+ exchanger SOS1 plays a major role in the salt tolerance of rice by controlling Na+ homeostasis and possibly contributing to the sensing of sodicity stress.
- Publication
Plant Physiology, 2019, Vol 180, Issue 2, p1046
- ISSN
0032-0889
- Publication type
Article
- DOI
10.1104/pp.19.00324