Soil bacteria confer plant salt tolerance by tissue-specific regulation of the sodium transporter HKT1
Soil bacteria confer plant salt tolerance by tissue-specific regulation of the sodium transporter HKT1
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DOI：
10.1094/mpmi-21-6-0737
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发表时间：
2008-06-01
影响因子：
3.5
通讯作者：
Pare, Paul W.
中科院分区：
文献类型：
--
作者：
Zhang, Huiming;Kim, Mi-Seong;Pare, Paul W.
高钠（Na+）会降低植物生长，从而降低农业生产力。离子转运蛋白高亲和力K+转运蛋白（HKT）1控制Na+在根中的输入，但HKT 1的功能障碍或过度表达未能增加耐盐性，引起了关于HKT 1在调节Na+稳态中的作用的问题。在这里，我们报告，组织特异性调节HKT 1的土壤细菌枯草芽孢杆菌GB 03赋予拟南芥耐盐性。在盐胁迫（100 mM NaCl）下，GB 03同时下调和上调HKT 1在根和芽中的表达，导致整个植物中Na+的积累低于对照。与HKT 1参与GB 03诱导的耐盐性一致，GB 03未能拯救盐胁迫的athkt 1突变体，使其免于叶生长受阻和总Na+升高，而盐胁迫的Na+输出突变体sos 3显示出GB 03诱导的耐盐性，具有增强的芽和根生长以及降低的总Na+。这些结果表明，HKT 1的组织特异性调节对于管理盐胁迫植物中的Na+稳态是至关重要的，并且强调了植物-微生物相互作用的广度和复杂性。
Elevated sodium (Na+) decreases plant growth and, thereby, agricultural productivity. The ion transporter high-affinity K+ transporter (HKT)1 controls Na+ import in roots, yet dysfunction or overexpression of HKT1 fails to increase salt tolerance, raising questions as to HKT1's role in regulating Na+ homeostasis. Here, we report that tissue-specific regulation of HKT1 by the soil bacterium Bacillus subtilis GB03 confers salt tolerance in Arabidopsis thaliana. Under salt stress (100 mM NaCl), GB03 concurrently down- and upregulates HKT1 expression in roots and shoots, respectively, resulting in lower Na+ accumulation throughout the plant compared with controls. Consistent with HKT1 participation in GB03-induced salt tolerance, GB03 fails to rescue salt-stressed athkt1 mutants from stunted foliar growth and elevated total Na+ whereas salt-stressed Na+ export mutants sos3 show GB03-induced salt tolerance with enhanced shoot and root growth as well as reduced total Na+. These results demonstrate that tissue-specific regulation of HKT1 is critical for managing Na+ homeostasis in salt-stressed plants, as well as underscore the breadth and sophistication of plant-microbe interactions.