首页> 美国卫生研究院文献>Journal of Experimental Botany >Haem oxygenase modifies salinity tolerance in Arabidopsis by controlling K+ retention via regulation of the plasma membrane H+-ATPase and by altering SOS1 transcript levels in roots
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Haem oxygenase modifies salinity tolerance in Arabidopsis by controlling K+ retention via regulation of the plasma membrane H+-ATPase and by altering SOS1 transcript levels in roots

机译:血红素加氧酶通过调节质膜H + -ATPase和改变根系中的SOS1转录水平来控制K +保留从而改变拟南芥的耐盐性

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摘要

Reactive oxygen species (ROS) production is a common denominator in a variety of biotic and abiotic stresses, including salinity. In recent years, haem oxygenase (HO; EC 1.14.99.3) has been described as an important component of the antioxidant defence system in both mammalian and plant systems. Moreover, a recent report on Arabidopsis demonstrated that HO overexpression resulted in an enhanced salinity tolerance in this species. However, physiological mechanisms and downstream targets responsible for the observed salinity tolerance in these HO mutants remain elusive. To address this gap, ion transport characteristics (K+ and H+ fluxes and membrane potentials) and gene expression profiles in the roots of Arabidopsis thaliana HO-overexpressing (35S:HY1-1/2/3/4) and loss-of-function (hy-100, ho2, ho3, and ho4) mutants were compared during salinity stress. Upon acute salt stress, HO-overexpressing mutants retained more K+ (less efflux), and exhibited better membrane potential regulation (maintained more negative potential) and higher H+ efflux activity in root epidermis, compared with loss-of-function mutants. Pharmacological experiments suggested that high activity of the plasma membrane H+-ATPase in HO overexpressor mutants provided the proton-motive force required for membrane potential maintenance and, hence, better K+ retention. The gene expression analysis after 12h and 24h of salt stress revealed high expression levels of H+-ATPases (AHA1/2/3) and Na+/H+ antiporter [salt overly sensitive1 (SOS1)] transcripts in the plasma membrane of HO overexpressors. It is concluded that HO modifies salinity tolerance in Arabidopsis by controlling K+ retention via regulation of the plasma membrane H+-ATPase and by altering SOS1 transcript levels in roots.
机译:活性氧(ROS)的产生是各种生物和非生物胁迫(包括盐分)中的共同特征。近年来,血红素加氧酶(HO; EC 1.14.99.3)已被描述为哺乳动物和植物系统中抗氧化防御系统的重要组成部分。此外,最近有关拟南芥的报告表明,HO的过表达导致该物种的盐分耐受性增强。然而,生理机制和下游目标负责这些HO突变体中观察到的盐度耐受性仍然难以捉摸。为了解决这个空白,拟南芥HO过表达(35S:HY1)根中的离子转运特性(K + 和H + 通量和膜电位)和基因表达谱-1/2/3/4)和功能丧失(hy-100,ho2,ho3和ho4)突变体在盐度胁迫下进行了比较。在急性盐胁迫下,高表达HO的突变体保留更多的K + (较少的外排),并表现出更好的膜电位调节(保持更多的负电位)和更高的H + 外排活性与功能丧失的突变体相比药理实验表明,HO过表达突变体中质膜H + -ATPase的高活性提供了维持膜电位所需的质子动力,因此具有更好的K + 保留。盐胁迫12h和24h后的基因表达分析表明,H + -ATPases(AHA1 / 2/3)和Na + / H +高表达 HO过表达子质膜中的反转运蛋白[盐过度敏感1(SOS1)]转录本。结论是HO通过调节质膜H + -ATPase并改变根中的SOS1转录水平来控制K + 保留,从而改变了拟南芥的耐盐性。

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