Jasmonic acid alleviates cadmium toxicity in Arabidopsis via suppression of cadmium uptake and translocation
Jasmonic acid alleviates cadmium toxicity in Arabidopsis via suppression of cadmium uptake and translocation
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DOI：
10.1111/jipb.12801
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发表时间：
2020-02-01
影响因子：
11.4
通讯作者：
Zheng, Shao Jian
中科院分区：
文献类型：
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作者：
Lei, Gui Jie;Sun, Li;Zheng, Shao Jian
茉莉酸（JA）被认为参与了植物对镉（Cd）胁迫的响应，但其分子机制尚不清楚。在这里，我们表明，镉处理迅速诱导基因的表达，促进内源JA合成，随后增加JA浓度在拟南芥根。此外，外源茉莉酸甲酯（MeJA）通过降低根细胞液和地上部中Cd浓度，降低促进Cd吸收和远距离运输的AtIRT1、AtHMA2和AtHMA4基因的表达，抑制Cd诱导的新叶失绿。相反，JA合成的关键基因AtAOS的突变，大大增强了AtIRT1，AtHMA2和AtHMA4的表达，增加了镉在根和芽的浓度，并赋予增加的敏感性镉。外源MeJA恢复增强的镉敏感性的ataos突变体，但不是atcoi1，JA受体突变体。此外，外源MeJA降低了镉胁迫下拟南芥根尖的NO水平。总之，我们的研究结果表明，镉诱导的JA行为通过JA信号通路和NO水平的影响，积极限制镉积累和减轻镉毒性，通过抑制基因的表达，促进镉的吸收和长距离运输。
Jasmonic acid (JA) is thought to be involved in plant responses to cadmium (Cd) stress, but the underlying molecular mechanisms are poorly understood. Here, we show that Cd treatment rapidly induces the expression of genes promoting endogenous JA synthesis, and subsequently increases the JA concentration in Arabidopsis roots. Furthermore, exogenous methyl jasmonate (MeJA) alleviates Cd-generated chlorosis of new leaves by decreasing the Cd concentration in root cell sap and shoot, and decreasing the expression of the AtIRT1, AtHMA2 and AtHMA4 genes promoting Cd uptake and long-distance translocation, respectively. In contrast, mutation of a key JA synthesis gene, AtAOS, greatly enhances the expression of AtIRT1, AtHMA2 and AtHMA4, increases Cd concentration in both roots and shoots, and confers increased sensitivity to Cd. Exogenous MeJA recovers the enhanced Cd-sensitivity of the ataos mutant, but not of atcoi1, a JA receptor mutant. In addition, exogenous MeJA reduces NO levels in Cd-stressed Arabidopsis root tips. Taken together, our results suggest that Cd-induced JA acts via the JA signaling pathway and its effects on NO levels to positively restrict Cd accumulation and alleviates Cd toxicity in Arabidopsis via suppression of the expression of genes promoting Cd uptake and long-distance translocation.