Ethylene and nitric oxide are involved in maintaining ion homeostasis in Arabidopsis callus under salt stress

Ethylene and nitric oxide are involved in maintaining ion homeostasis in Arabidopsis callus under salt stress
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乙烯和一氧化氮参与盐胁迫下拟南芥愈伤组织离子稳态的维持

DOI:
10.1007/s00425-009-0946-y
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发表时间:
2009-05
期刊:
影响因子:
4.3
通讯作者:
Wang, Huahua
Wang, Huahua
中科院分区:
生物学2区
文献类型:
--
作者:
Wang, Xiaomin;Liang, Xiaolei;Wan, Qi;Bi, Yurong;Wang, Huahua

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本研究探讨了乙烯在盐胁迫下拟南芥愈伤组织中一氧化氮(NO)介导的离子稳态保护作用。结果表明,乙烯不敏感突变体etr 1 -3对盐胁迫的敏感性高于野生型。在100 mM NaCl胁迫下,etr 1 -3愈伤组织的电解质渗漏率和Na(+)/K(+)比值均高于WT愈伤组织,但质膜H(+)-ATPase活性低于WT愈伤组织。外源1-氨基环丙烷-1-羧酸(ACC,乙烯前体)或硝普钠(SNP,NO供体)通过维持WT愈伤组织较低的Na(+)/K(+)比值和增加PM H(+)-ATP酶活性来减轻NaCl诱导的损伤,但对etr 1 -3愈伤组织无影响。在NaCl胁迫下,WT愈伤组织中的SNP作用被特异性NO清除剂或乙烯生物合成抑制剂减弱。在100 mM NaCl胁迫下,WT愈伤组织的NO积累和乙烯释放出现较早,NO的产生大大促进了乙烯的释放。此外,乙烯诱导盐胁迫下质膜H(+)-ATPase基因的表达。恢复实验表明NaCl诱导的损伤是可逆的,WT愈伤组织中Na(+)/K(+)比值和PM H(+)-ATPase活性恢复相似。这些结果表明,乙烯和NO协同刺激质膜H(+)-ATP酶活性,调节离子稳态以提高植物的耐盐性,乙烯可能是NO作用的下游信号分子之一。
In the present study, the role of ethylene in nitric oxide (NO)-mediated protection by modulating ion homeostasis in Arabidopsis callus under salt stress was investigated. Results showed that the ethylene-insensitive mutant etr1-3 was more sensitive to salt stress than the wild type (WT). Under 100 mM NaCl, etr1-3 callus displayed a greater electrolyte leakage and Na(+)/K(+) ratio but a lower plasma membrane (PM) H(+)-ATPase activity compared to WT callus. Application of exogenous 1-aminocyclopropane-1-carboxylic acid (ACC, an ethylene precursor) or sodium nitroprusside (SNP, a NO donor) alleviated NaCl-induced injury by maintaining a lower Na(+)/K(+) ratio and an increased PM H(+)-ATPase activity in WT callus but not in etr1-3 callus. The SNP actions in NaCl stress were attenuated by a specific NO scavenger or an ethylene biosynthesis inhibitor in WT callus. Under 100 mM NaCl, the NO accumulation and ethylene emission appeared at early time, and NO production greatly stimulated ethylene emission in WT callus. In addition, ethylene induced the expression of PM H(+)-ATPase genes under salt stress. The recovery experiment showed that NaCl-induced injury was reversible, as signaled by the similar recovery of Na(+)/K(+) ratio and PM H(+)-ATPase activity in WT callus. Taken together, the results indicate that ethylene and NO cooperate in stimulating PM H(+)-ATPase activity to modulate ion homeostasis for salt tolerance, and ethylene may be a part of the downstream signal molecular in NO action.
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