Tolerance to high soil [Na(+)] involves processes in many different parts of the plant, and is manifested in a wide range of specializations at disparate levels of organization, such as gross morphology, membrane transport, biochemistry and gene transcription. Multiple adaptations to high [Na(+)] operate concurrently within a particular plant, and mechanisms of tolerance show large taxonomic variation. These mechanisms can occur in all cells within the plant, or can occur in specific cell types, reflecting adaptations at two major levels of organization: those that confer tolerance to individual cells, and those that contribute to tolerance not of cells per se, but of the whole plant. Salt-tolerant cells can contribute to salt tolerance of plants; but we suggest that equally important in a wide range of conditions are processes involving the management of Na(+) movements within the plant. These require specific cell types in specific locations within the plant catalysing transport in a coordinated manner. For further understanding of whole plant tolerance, we require more knowledge of cell-specific transport processes and the consequences of manipulation of transporters and signalling elements in specific cell types.

HKT-type transporters appear to play key roles in Na + accumulation and salt sensitivity in plants. In Arabidopsis HKT1;1 has been proposed to influx Na + into roots, recirculate Na + in the phloem and control root : shoot allocation of Na + . We tested these hypotheses using 22 Na + flux measurements and ion accumulation assays in an hkt1;1 mutant and demonstrated that AtHKT1;1 contributes to the control of both root accumulation of Na + and retrieval of Na + from the xylem, but is not involved in root influx or recirculation in the phloem. Mathematical modelling indicated that the effects of the hkt1;1 mutation on root accumulation and xylem retrieval were independent. Although AtHKT1;1 has been implicated in regulation of K + transport and the hkt1;1 mutant showed altered net K + accumulation, 86 Rb + uptake was unaffected by the hkt1;1 mutation. The hkt1;1 mutation has been shown previously to rescue growth of the sos1 mutant on low K + ; however, HKT1;1 knockout did not alter K + or 86 Rb + accumulation in sos1.

Arabidopsis is frequently used as a genetic model in plant salt tolerance studies, however, its physiological responses to salinity remain poorly characterized. This study presents a characterization of initial Na ϩ entry and the effects of Ca 2ϩ on plant growth and net Na ϩ accumulation in saline conditions. Unidirectional Na ϩ influx was measured carefully using very short influx times in roots of 12-d-old seedlings. Influx showed three components with distinct sensitivities to Ca 2ϩ , diethylpyrocarbonate, and osmotic pretreatment. Pharmacological agents and known mutants were used to test the contribution of different transport pathways to Na ϩ uptake. Influx was stimulated by 4-aminobutyric acid and glutamic acid; was inhibited by flufenamate, quinine, and cGMP; and was insensitive to modulators of K ϩ and Ca 2ϩ channels. Influx did not differ from wild type in akt1 and hkt1 insertional mutants. These data suggested that influx was mediated by several different types of nonselective cation channels. Na ϩ accumulation in plants grown in 50 mm NaCl was strongly reduced by increasing Ca 2ϩ activity (from 0.05-3.0 mm), and plant survival was improved. However, plant biomass was not affected by shoot Na ϩ concentration, suggesting that in Arabidopsis Na ϩ toxicity is not dependent on shoot Na ϩ accumulation. These data suggest that Arabidopsis is a good model for investigation of Na ϩ transport, but may be of limited utility as a model for the study of Na ϩ toxicity.

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