A cadmium stress-responsive gene AtFC1 confers plant tolerance to cadmium toxicity.
A cadmium stress-responsive gene AtFC1 confers plant tolerance to cadmium toxicity.
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DOI：
10.1186/s12870-017-1141-0
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发表时间：
2017-10-30
影响因子：
5.3
通讯作者：
Yang ZM
中科院分区：
文献类型：
--
作者：
Song J;Feng SJ;Chen J;Zhao WT;Yang ZM
非必需微量金属如镉（Cd）对植物是有毒的。虽然一些植物已经开发出复杂的策略，通过多种途径来处理吸收的镉，镉耐性背后的调控机制还没有完全理解。亚铁螯合酶-1（FC 1，EC 4.99.1.1）是血红素生物合成的末端酶，催化亚铁离子插入原卟啉IX。最近的研究表明，FC 1参与了几个生理过程。然而，它与植物非生物胁迫反应相关的生物学功能却知之甚少。在这项研究中，我们表明，AtFC 1的转录激活镉暴露。AtFC 1过表达（35 S：：FC 1）株系积累了比野生型更多的Cd和非蛋白巯基化合物，并赋予植物对Cd胁迫的耐受性，提高了初生根伸长、生物量和叶绿素（Chl）含量，降低了与H2 O2、O·2-和过氧化物相关的氧化程度。而功能突变体fc 1的AtFC 1缺失则表现出对Cd胁迫的敏感性。外源血红素，AtFC 1的产品，部分拯救镉诱导的毒性表型的fc 1突变体，通过改善幼苗的生长，谷胱甘肽（GSH）和植物螯合素（PC）的产生，和GSH/PC合成的基因表达（如GSH 1，GSH 2，PCS 1，和PCS 2）。为了研究AtFC 1基因调控拟南芥镉胁迫响应的机制，对镉胁迫下fc 1突变体的转录组进行了分析。我们的数据表明，AtFC 1的功能障碍导致913个基因特异性上调和522个基因下调fc 1突变体暴露于镉。一些基因参与金属转运蛋白，镉诱导的氧化应激反应，解毒。这些结果表明AtFC 1可能是植物对Cd胁迫耐受性的正向调节因子。本研究将拓宽对FC 1在介导植物对Cd胁迫响应中的作用的认识，并为进一步探索其下游基因提供基础。本文的在线版本（10.1186/s12870-017-1141-0）包含补充材料，可供授权用户使用。
Non-essential trance metal such as cadmium (Cd) is toxic to plants. Although some plants have developed elaborate strategies to deal with absorbed Cd through multiple pathways, the regulatory mechanisms behind the Cd tolerance are not fully understood. Ferrochelatase-1 (FC1, EC4.99.1.1) is the terminal enzyme of heme biosynthesis, catalyzing insertion of ferrous ion into protoporphyrin IX. Recent studies have shown that FC1 is involved in several physiological processes. However, its biological function associated with plant abiotic stress response is poorly understood. In this study, we showed that AtFC1 was transcriptionally activated by Cd exposure. AtFC1 overexpression (35S::FC1) lines accumulated more Cd and non-protein thiol compounds than wild-type, and conferred plant tolerance to Cd stress, with improved primary root elongation, biomass and chlorophyll (Chl) content, and low degree of oxidation associated with reduced H2O2, O·2- and peroxides. In contrast, the AtFC1 loss of functional mutant fc1 showed sensitivity to Cd stress. Exogenous provision of heme, the product of AtFC1, partially rescued the Cd-induced toxic phenotype of fc1 mutants by improving the growth of seedlings, generation of glutathione (GSH) and phytochelatins (PCs), and GSH/PCs-synthesized gene expression (e.g. GSH1, GSH2, PCS1, and PCS2). To investigate the mechanism leading to the AtFC1 regulating Cd stress response in Arabidopsis, a transcriptome of fc1 mutant plants under Cd stress was profiled. Our data showed that disfunction of AtFC1 led to 913 genes specifically up-regulated and 522 genes down-regulated in fc1 mutants exposed to Cd. Some of the genes are involved in metal transporters, Cd-induced oxidative stress response, and detoxification. These results indicate that AtFC1 would act as a positive regulator of plant tolerance to Cd stress. Our study will broaden our understanding of the role of FC1 in mediating plant response to Cd stress and provide a basis for further exploration of its downstream genes. The online version of this article (10.1186/s12870-017-1141-0) contains supplementary material, which is available to authorized users.