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Maintenance of K<sup>+</sup>/Na<sup>+</sup> Balance in the Roots of <i>Nitraria sibirica</i> Pall. in Response to NaCl Stress

Author:
Tang, Xiaoqian, Yang, Xiuyan, Li, Huanyong, Zhang, Huaxin
Source:
Forests 2018 v.9 no.10
ISSN:
1999-4907
Subject:
H-transporting ATP synthase, Nitraria, energy, enzyme inhibitors, plasma membrane, potassium, potassium channels, proton pump, protons, root meristems, salt stress, salt tolerance, seedlings, sodium, sodium chloride, sodium-hydrogen antiporter, tetraethylammonium compounds
Abstract:
Using Non-invasive Micro-test Technology (NMT), the Na+, K+ and H+ flux profiles in the root meristem regions were investigated in Nitraria sibirica Pall. seedlings under different NaCl concentrations. NaCl stress increased the K+ and Na+ contents in the roots of N. sibirica seedlings. NaCl stress significantly increased the steady Na+ efflux from the N. sibirica seedling roots. Steady K+ effluxes were measured in the control roots (without NaCl) and in the roots treated with 200 mM NaCl, and no significant differences were observed between the two treatments. The steady K+ efflux from roots treated with 400 mM NaCl decreased gradually. NaCl treatment significantly increased the H+ influx. Pharmacological experiments showed that amiloride and sodium vanadate significantly inhibited the Na+ efflux and H+ influx, suggesting that the Na+ efflux was mediated by a Na+/H+ antiporter using energy provided by plasma membrane H+-ATPase. The NaCl-induced root K+ efflux was inhibited by the K+ channel inhibitor tetraethylammonium chloride (TEA), and was significantly increased by the H+-ATPase inhibitor sodium vanadate. The NaCl-induced K+ efflux was mediated by depolarization-activated outward-rectifying K+ channels and nonselective cation channels (NSCCs). Under salt stress, N. sibirica seedlings showed increased Na+ efflux due to increased plasma membrane H+-ATPase and Na+/H+ antiporter activity. High H+ pump activity not only restricts the Na+ influx through NSCCs, but also limits K+ leakage through outward-rectifying K+ channels and NSCCs, leading to maintenance of the K+/Na+ balance and higher salt tolerance.
Agid:
6488751