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首页> 外文期刊>Science >SODIUM-DRIVEN POTASSIUM UPTAKE BY THE PLANT POTASSIUM TRANSPORTER HKT1 AND MUTATIONS CONFERRING SALT TOLERANCE
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SODIUM-DRIVEN POTASSIUM UPTAKE BY THE PLANT POTASSIUM TRANSPORTER HKT1 AND MUTATIONS CONFERRING SALT TOLERANCE

机译:植物钾转运体HKT1吸收钠驱动的钾和赋予耐盐性的突变

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摘要

Sodium (Na+) at high millimolar concentrations in soils is toxic to most higher plants and severely reduces agricultural production worldwide. However, the molecular mechanisms for plant Na+ uptake remain unknown. Here, the wheat root high-affinity potassium (K+) uptake transporter HKT1 was shown to function as a high-affinity K+-Na+ cotransporter. High-affinity K+ uptake was activated by micromolar Na+ concentrations; moreover, high-affinity Na+ uptake was activated by K+ (half-activation constant, 2.8 mu M K+). However, at physiologically detrimental concentrations of Na+, K+ accumulation mediated by HKT1 was blocked and low-affinity Na+ uptake occurred (Michaelis constant, similar to 16 mM Na+), which correlated to Na+ toxicity in plants. Point mutations in the sixth putative transmembrane domain of HKT1 that increase Na+ tolerance were isolated with the use of yeast as a screening system. Na+ uptake and Na+ inhibition of K+ accumulation indicate a possible role for HKT1 in physiological Na+ toxicity in plants.
机译:土壤中高浓度的钠(Na +)对大多数高等植物有毒,并严重降低了全球的农业生产。然而,植物Na +吸收的分子机制仍然未知。在这里,小麦根高亲和力钾(K +)吸收转运蛋白HKT1被显示为高亲和力K + -Na +共转运蛋白。高亲和力的K +摄取被微摩尔浓度的Na +激活;此外,高亲和力的Na +吸收被K +激活(半激活常数为2.8μM K +)。然而,在生理有害的Na +浓度下,HKT1介导的K +积累被阻断,并且发生了低亲和性Na +吸收(Michaelis常数,类似于16 mM Na +),这与植物中的Na +毒性相关。通过使用酵母作为筛选系统分离了HKT1第六个假定的跨膜结构域中增加Na +耐受性的点突变。 Na +吸收和Na +抑制K +积累表明HKT1在植物生理Na +毒性中可能发挥作用。

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