有毒的类金属砷在环境中普遍存在,对几乎所有生物都构成威胁。然而,植物激素调节砷抗性的机制尚不清楚。因此,我们根据转录组测序结果分析了多种植物激素,内容更改,和砷胁迫下相关的突变体生长。我们发现乙烯是拟南芥对砷反应的关键植物激素。进一步的研究表明,乙烯过量产生的突变体eto1-1产生较少的丙二醛(MDA),与野生型相比,砷胁迫下的H2O2和O2•-而对乙烯不敏感的突变体ein2-5显示出相反的模式。与野生型相比,eto1-1积累了较少量的砷和较大量的非蛋白质硫醇。此外,直接的乙烯前体,1-氨基环丙烷-1-羧酸(ACC),增强对宽型砷的抗性,但在解毒能力受损的突变体中不存在(即,cad1-3,pad2-1,abcc1abcc2),这证实了乙烯通过增强砷的螯合作用来调节砷的解毒作用。ACC还上调了参与砷解毒的基因的表达,其中ABCC2被乙烯主转录因子乙烯不敏感3(EIN3)直接转录激活。总的来说,我们的研究表明,乙烯是通过在生理和分子水平上减少砷积累和促进砷解毒来增强抗砷性的关键植物激素。
The toxic metalloid arsenic is prevalent in the environment and poses a threat to nearly all organisms. However, the mechanism by which phytohormones modulate arsenic resistance is not well-understood. Therefore, we analyzed multiple phytohormones based on the results of transcriptome sequencing, content changes, and related mutant growth under arsenic stress. We found that ethylene was the key phytohormone in Arabidopsis thaliana response to arsenic. Further investigation showed the ethylene-overproducing mutant eto1-1 generated less malondialdehyde (MDA), H2O2, and O2•- under arsenic stress compared to wild-type, while the ethylene-insensitive mutant ein2-5 displayed opposite patterns. Compared to wild-type, eto1-1 accumulated a smaller amount of arsenic and a larger amount of non-protein thiols. Additionally, the immediate ethylene precursor, 1-aminocyclopropane-1-carboxylic acid (ACC), enhanced resistance to arsenic in wide-type, but not in mutants with impaired detoxification capability (i.e., cad1-3, pad2-1, abcc1abcc2), which confirmed that ethylene regulated arsenic detoxification by enhancing arsenic chelation. ACC also upregulated the expression of gene(s) involved in arsenic detoxification, among which ABCC2 was directly transcriptionally activated by the ethylene master transcription factor ethylene-insensitive 3 (EIN3). Overall, our study shows that ethylene is the key phytohormone to enhance arsenic resistance by reducing arsenic accumulation and promoting arsenic detoxification at both physiological and molecular levels.