42K analysis of sodium-induced potassium efflux in barley: mechanism and relevance to salt tolerance
Article first published online: 28 JAN 2010
© The Authors (2010). Journal compilation © New Phytologist Trust (2010)
Volume 186, Issue 2, pages 373–384, April 2010
How to Cite
Britto, D. T., Ebrahimi-Ardebili, S., Hamam, A. M., Coskun, D. and Kronzucker, H. J. (2010), 42K analysis of sodium-induced potassium efflux in barley: mechanism and relevance to salt tolerance. New Phytologist, 186: 373–384. doi: 10.1111/j.1469-8137.2009.03169.x
- Issue published online: 25 MAR 2010
- Article first published online: 28 JAN 2010
- Received: 28 October 2009, Accepted: 28 November 2009
- barley (Hordeum vulgare);
- ion channels;
- membrane integrity;
- potassium transport;
- salt stress
- •Stimulation of potassium (K+) efflux by sodium (Na+) has been the subject of much recent attention, and its mechanism has been attributed to the activities of specific classes of ion channels.
- •The short-lived radiotracer 42K+ was used to test this attribution, via unidirectional K+-flux analysis at the root plasma membrane of intact barley (Hordeum vulgare), in response to NaCl, KCl, NH4Cl and mannitol, and to channel inhibitors.
- •Unidirectional K+ efflux was strongly stimulated by NaCl, and K+ influx strongly suppressed. Both effects were ameliorated by elevated calcium (Ca2+). As well, K+ efflux was strongly stimulated by KCl, NH4Cl and mannitol , and NaCl also stimulated 13NH4+ efflux. The Na+-stimulated K+ efflux was insensitive to cesium (Cs+) and pH 4.2, weakly sensitive to the K+-channel blocker tetraethylammonium (TEA+) and quinine, and moderately sensitive to zinc (Zn2+) and lanthanum (La3+).
- •We conclude that the stimulated efflux is: specific neither to Na+ as effector nor K+ as target; composed of fluxes from both cytosol and vacuole; mediated neither by outwardly-rectifying K+ channels nor nonselective cation channels; attributable, alternatively, to membrane disintegration brought about by ionic and osmotic components; of limited long-term significance, unlike the suppression of K+ influx by Na+, which is a greater threat to K+ homeostasis under salt stress.