Shoot Na⁺ Exclusion and Increased Salinity Tolerance Engineered by Cell Type-Specific Alteration of Na⁺ Transport in Arabidopsis

Soil salinity affects large areas of cultivated land, causing significant reductions in crop yield globally. The Na⁺ toxicity of many crop plants is correlated with overaccumulation of Na⁺ in the shoot. We have previously suggested that the engineering of Na⁺ exclusion from the shoot could be achiev...

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Veröffentlicht in:The Plant cell 2009-07, Vol.21 (7), p.2163-2178
Hauptverfasser: Møller, Inge S, Gilliham, Matthew, Jha, Deepa, Mayo, Gwenda M, Roy, Stuart J, Coates, Juliet C, Haseloff, Jim, Tester, Mark
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Sprache:eng
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Zusammenfassung:Soil salinity affects large areas of cultivated land, causing significant reductions in crop yield globally. The Na⁺ toxicity of many crop plants is correlated with overaccumulation of Na⁺ in the shoot. We have previously suggested that the engineering of Na⁺ exclusion from the shoot could be achieved through an alteration of plasma membrane Na⁺ transport processes in the root, if these alterations were cell type specific. Here, it is shown that expression of the Na⁺ transporter HKT1;1 in the mature root stele of Arabidopsis thaliana decreases Na⁺ accumulation in the shoot by 37 to 64%. The expression of HKT1;1 specifically in the mature root stele is achieved using an enhancer trap expression system for specific and strong overexpression. The effect in the shoot is caused by the increased influx, mediated by HKT1;1, of Na⁺ into stelar root cells, which is demonstrated in planta and leads to a reduction of root-to-shoot transfer of Na⁺. Plants with reduced shoot Na⁺ also have increased salinity tolerance. By contrast, plants constitutively expressing HKT1;1 driven by the cauliflower mosaic virus 35S promoter accumulated high shoot Na⁺ and grew poorly. Our results demonstrate that the modification of a specific Na⁺ transport process in specific cell types can reduce shoot Na⁺ accumulation, an important component of salinity tolerance of many higher plants.
ISSN:1040-4651
1532-298X
DOI:10.1105/tpc.108.064568