College of Life Sciences, Nanjing Agricultural University, Nanjing 210095, China.
State Key Laboratory of Crop Stress Adaptation and Improvement, School of Life Sciences, Henan University, Kaifeng 475004, China.
Ecotoxicol Environ Saf. 2024 Aug;281:116644. doi: 10.1016/j.ecoenv.2024.116644. Epub 2024 Jun 28.
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), HO, and O 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.
有毒类金属砷在环境中普遍存在，对几乎所有生物体构成威胁。然而，植物激素调节砷抗性的机制还不清楚。因此，我们基于转录组测序、含量变化和相关突变体在砷胁迫下的生长结果分析了多种植物激素。我们发现乙烯是拟南芥响应砷的关键植物激素。进一步的研究表明，与野生型相比，乙烯过量产生突变体 eto1-1 在砷胁迫下产生的丙二醛（MDA）、HO 和 O 较少，而乙烯不敏感突变体 ein2-5 则表现出相反的模式。与野生型相比，eto1-1 积累的砷较少，非蛋白巯基较多。此外，乙烯的直接前体 1-氨基环丙烷-1-羧酸（ACC）增强了野生型对砷的抗性，但在解毒能力受损的突变体（即 cad1-3、pad2-1、abcc1abcc2）中没有增强抗性，这证实了乙烯通过增强砷螯合作用来调节砷解毒。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，乙烯是增强砷抗性的关键植物激素，它通过减少砷积累和促进砷解毒来提高生理和分子水平的砷抗性。
