Salt-Sensitive Signaling Networks in the Mediation of K(+)/Na(+) Homeostasis Gene Expression in Glycyrrhiza uralensis Roots.
Salt-Sensitive Signaling Networks in the Mediation of K(+)/Na(+) Homeostasis Gene Expression in Glycyrrhiza uralensis Roots.
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盐敏感信号网络介导甘草根 K/Na 稳态基因表达
DOI：
10.3389/fpls.2017.01403
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发表时间：
2017
影响因子：
5.6
通讯作者：
Chen S
中科院分区：
文献类型：
--
作者：
Lang T;Deng S;Zhao N;Deng C;Zhang Y;Zhang Y;Zhang H;Sa G;Yao J;Wu C;Wu Y;Deng Q;Lin S;Xia J;Chen S
我们研究了盐敏感信号分子对离子通量和基因表达的影响，K+/Na+稳态的多年生草本植物，甘草，在短期NaCl胁迫（100 mM，24 h）。盐处理引起根细胞比叶细胞更明显的Na+积累。Na+主要分布在液泡中。暴露于NaCl的根表现出细胞外ATP（eATP），胞内Ca 2+，H2 O2，和NO的水平增加。稳态流量记录显示，这些盐敏感的信号分子增强NaCl响应的Na+外流，由于激活Na+/H+逆向运输系统在质膜（PM）。此外，盐引起的K+外流，这是介导的去极化激活的阳离子通道，减少与另外的Ca 2+，H2 O2，NO，和eATP。这些分子的盐适应性效应（Na+排出和K+维持）被药理学试剂降低，包括LaCl 3（PM Ca 2+通道抑制剂）、DMTU（活性氧清除剂）、cPTIO（NO清除剂）或PPADS（动物PM嘌呤P2受体的拮抗剂）。RT-qPCR结果表明，盐胁迫下根中质膜Na+/H+逆向转运系统的激活可能是由于编码质膜Na+/H+逆向转运蛋白的两个基因GuSOS 1和GuAHA的表达上调所致，这两个基因分别编码盐过度敏感1（SOS 1）和H+-ATPase。这些盐敏感激动剂之间存在明显的相互作用，促进了盐敏感信号通路基因的转录。乌拉尔根例如，Ca 2+，H2 O2，NO和eATP促进GuSOS 3（盐过度敏感3）和/或GuCIPK（CBL-interacting protein kinase）的转录，以激活盐渍化拟南芥根中主要的Ca 2 +-SOS信号通路。eATP是G. uralensis，增加GuSOS 3、GuCIPK、GuRbohD（呼吸爆发氧化酶同源蛋白D）、GuNIR（硝酸还原酶）、GuMAPK 3和GuMAPK 6（促分裂原活化蛋白激酶3和6）的转录。此外，GuMAPK 3和GuMAPK 6的表达水平在NaCl胁迫下被H2 O2增强。乌拉尔根我们的研究结果表明，eATP触发下游组件，并与Ca 2+，H2 O2，NO信号相互作用，以维持K+/Na+稳态。我们认为NaCl胁迫下G.乌拉尔根
We investigated the effects of salt-sensitive signaling molecules on ionic fluxes and gene expression related to K+/Na+ homeostasis in a perennial herb, Glycyrrhiza uralensis, during short-term NaCl stress (100 mM, 24 h). Salt treatment caused more pronounced Na+ accumulation in root cells than in leaf cells. Na+ ions were mostly compartmentalized in vacuoles. Roots exposed to NaCl showed increased levels of extracellular ATP (eATP), cytosolic Ca2+, H2O2, and NO. Steady-state flux recordings revealed that these salt-sensitive signaling molecules enhanced NaCl-responsive Na+ efflux, due to the activated Na+/H+ antiport system in the plasma membrane (PM). Moreover, salt-elicited K+ efflux, which was mediated by depolarization-activated cation channels, was reduced with the addition of Ca2+, H2O2, NO, and eATP. The salt-adaptive effects of these molecules (Na+ extrusion and K+ maintenance) were reduced by pharmacological agents, including LaCl3 (a PM Ca2+ channel inhibitor), DMTU (a reactive oxygen species scavenger), cPTIO (an NO scavenger), or PPADS (an antagonist of animal PM purine P2 receptors). RT-qPCR data showed that the activation of the PM Na+/H+ antiport system in salinized roots most likely resulted from the upregulation of two genes, GuSOS1 and GuAHA, which encoded the PM Na+/H+ antiporter, salt overly sensitive 1 (SOS1), and H+-ATPase, respectively. Clear interactions occurred between these salt-sensitive agonists to accelerate transcription of salt-responsive signaling pathway genes in G. uralensis roots. For example, Ca2+, H2O2, NO, and eATP promoted transcription of GuSOS3 (salt overly sensitive 3) and/or GuCIPK (CBL-interacting protein kinase) to activate the predominant Ca2+-SOS signaling pathway in salinized liquorice roots. eATP, a novel player in the salt response of G. uralensis, increased the transcription of GuSOS3, GuCIPK, GuRbohD (respiratory burst oxidase homolog protein D), GuNIR (nitrate reductase), GuMAPK3, and GuMAPK6 (the mitogen-activated protein kinases 3 and 6). Moreover, GuMAPK3 and GuMAPK6 expression levels were enhanced by H2O2 in NaCl-stressed G. uralensis roots. Our results indicated that eATP triggered downstream components and interacted with Ca2+, H2O2, and NO signaling to maintain K+/Na+ homeostasis. We propose that a multiple signaling network regulated K+/Na+ homeostasis in NaCl-stressed G. uralensis roots.
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