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内-β甘露聚糖酶 MAN7 通过调节拟南芥根细胞壁结合能力来促进镉耐受性。

The endo-beta mannase MAN7 contributes to cadmium tolerance by modulating root cell wall binding capacity in Arabidopsis thaliana.

机构信息

State Key Laboratory of Soil and Sustainable Agriculture, Institute of Soil Science, Chinese Academy of Sciences, Nanjing, 210008, China.

University of Chinese Academy of Sciences, Beijing, 100049, China.

出版信息

J Integr Plant Biol. 2023 Jul;65(7):1670-1686. doi: 10.1111/jipb.13487. Epub 2023 Apr 21.

Abstract

The heavy metal cadmium (Cd) is detrimental to crop growth and threatens human health through the food chain. To cope with Cd toxicity, plants employ multiple strategies to decrease Cd uptake and its root-to-shoot translocation. However, genes that participate in the Cd-induced transcriptional regulatory network, including those encoding transcription factors, remain largely unidentified. In this study, we demonstrate that ENDO-BETA-MANNASE 7 (MAN7) is necessary for the response of Arabidopsis thaliana to toxic Cd levels. We show that MAN7 is responsible for mannase activity and modulates mannose content in the cell wall, which plays a role in Cd compartmentalization in the cell wall under Cd toxicity conditions. Additionally, the repression of root growth by Cd was partially reversed via exogenous application of mannose, suggesting that MAN7-mediated cell wall Cd redistribution depends on the mannose pathway. Notably, we identified a basic leucine zipper (bZIP) transcription factor, bZIP44, that acts upstream of MAN7 in response to Cd toxicity. Transient dual-luciferase assays indicated that bZIP44 directly binds to the MAN7 promoter region and activates its transcription. Loss of bZIP44 function was associated with greater sensitivity to Cd treatment and higher accumulation of the heavy metal in roots and shoots. Moreover, MAN7 overexpression relieved the inhibition of root elongation seen in the bzip44 mutant under Cd toxicity conditions. This study thus reveals a pathway showing that MAN7-associated Cd tolerance in Arabidopsis is controlled by bZIP44 upon Cd exposure.

摘要

重金属镉(Cd)会损害作物生长,并通过食物链威胁人类健康。为了应对 Cd 毒性,植物采用多种策略来减少 Cd 的吸收及其从根部向地上部的转运。然而,参与 Cd 诱导的转录调控网络的基因,包括那些编码转录因子的基因,在很大程度上仍未被识别。在这项研究中,我们证明了内-β-甘露聚糖酶 7(MAN7)是拟南芥应对有毒 Cd 水平所必需的。我们表明,MAN7 负责甘露聚糖酶活性,并调节细胞壁中的甘露糖含量,这在 Cd 毒性条件下细胞壁中 Cd 的区室化中发挥作用。此外,Cd 对根生长的抑制作用可以通过外源性甘露糖部分逆转,这表明 MAN7 介导的细胞壁 Cd 再分配依赖于甘露糖途径。值得注意的是,我们鉴定了一个碱性亮氨酸拉链(bZIP)转录因子 bZIP44,它在响应 Cd 毒性时位于 MAN7 的上游。瞬时双荧光素酶测定表明,bZIP44 直接结合 MAN7 启动子区域并激活其转录。bZIP44 功能丧失与对 Cd 处理更敏感以及根和地上部重金属积累增加有关。此外,MAN7 过表达缓解了 bzip44 突变体在 Cd 毒性条件下根伸长受到的抑制。因此,这项研究揭示了一条途径,表明在 Cd 暴露下,拟南芥中与 MAN7 相关的 Cd 耐受性受 bZIP44 控制。

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