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Published on December 18, 2003; 10.1104/pp.103.030361

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Received July 26, 2003
Returned for revision August 31, 2003
Accepted September 22, 2003

Regulation of K+ Transport in Tomato Roots by the TSS1 Locus. Implications in Salt Tolerance

Lourdes Rubio , Abel Rosado , Adolfo Linares-Rueda , Omar Borsani , María J. García-Sánchez , Victoriano Valpuesta , José A. Fernández , and Miguel A. Botella *

Departamento de Biología Vegetal (L.R., A.L.-R., M.J.G.-S., J.A.F.) and Departamento de Biología Molecular y Bioquímica (A.R., V.V., M.A.B.), Universidad de Málaga, 29071 Málaga, Spain; and Departamento de Biología Vegetal, Laboratorio de Bioquímica, Facultad de Agronomía, Avda Garzon 780, 12900 Montevideo, Uruguay (O.B.)

* Corresponding author; email: mabotella{at}uma.es.

The tss1 tomato (Lycopersicon esculentum) mutant exhibited reduced growth in low K+ and hypersensitivity to Na+ and Li+. Increased Ca2+ in the culture medium suppressed the Na+ hypersensitivity and the growth defect on low K+ medium of tss1 seedlings. Interestingly, removing NH4+ from the growth medium suppressed all growth defects of tss1, suggesting a defective NH4+-insensitive component of K+ transport. We performed electrophysiological studies to understand the contribution of the NH4+-sensitive and -insensitive components of K+ transport in wild-type and tss1 roots. Although at 1 mM Ca2+ we found no differences in affinity for K+ uptake between wild type and tss1 in the absence of NH4+, the maximum depolarization value was about one-half in tss1, suggesting that a set of K+ transporters is inactive in the mutant. However, these transporters became active by raising the external Ca2+ concentration. In the presence of NH4+, a reduced affinity for K+ was observed in both types of seedlings, but tss1 at 1 mM Ca2+ exhibited a 2-fold higher Km than wild type did. This defect was again corrected by raising the external concentration of Ca2+. Therefore, membrane potential measurements in root cells indicated that tss1 is affected in both NH4+-sensitive and -insensitive components of K+ transport at low Ca2+ concentrations and that this defective transport is rescued by increasing the concentration of Ca2+. Our results suggest that the TSS1 gene product is part of a crucial pathway mediating the beneficial effects of Ca2+ involved in K+ nutrition and salt tolerance.




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