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42 K analysis of sodium‐induced potassium efflux in barley: mechanism and relevance to salt tolerance
Author(s) -
Britto Dev T.,
EbrahimiArdebili Sasha,
Hamam Ahmed M.,
Coskun Devrim,
Kronzucker Herbert J.
Publication year - 2010
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/j.1469-8137.2009.03169.x
Subject(s) - efflux , chemistry , potassium , sodium , biophysics , ion transporter , mannitol , hordeum vulgare , cytosol , biochemistry , membrane , biology , botany , poaceae , organic chemistry , enzyme
Summary• 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 42 K + 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, NH 4 Cl 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 (Ca 2+ ). As well, K + efflux was strongly stimulated by KCl, NH 4 Cl and mannitol , and NaCl also stimulated 13 NH 4 + 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 (Zn 2+ ) and lanthanum (La 3+ ). • 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.