ANAC050 confers aluminium resistance by cooperating with secretion of organic acids and accumulation of cell wall hemicelluloses in plants

文献类型： 外文期刊

第一作者： Tao, Ye

作者： Tao, Ye;Li, Su;Liu, Yusong;Shen, Renfang;Zhu, Xiaofang;Tao, Ye;Li, Su;Shen, Renfang;Zhu, Xiaofang;Tao, Ye;Guo, Rui;Zhang, Qiang;Chen, Changzhao;Huang, Jiu

作者机构：

关键词： Al accumulation; Al toxicity; Arabidopsis; cell wall fixation; sensitive phenotype; transcription factor; transgenic line

期刊名称：PEDOSPHERE （ 影响因子：7.3； 五年影响因子：6.2 ）

ISSN： 1002-0160

年卷期： 2025 年 35 卷 2 期

页码：

收录情况： SCI

摘要： Aluminium (Al) toxicity is one of the key factors limiting crop output in acidic soils, but until now little has been known about how Al is regulated transcriptionally in plants. This study identified Arabidopsis NAC transcription factor ANAC050 in the regulation of Al tolerance. ANAC050 was located in the nucleus and displayed constitutive expression in the silique, flower, leaf, stem, and root, despite the fact that Al stress decreased its expression and protein accumulation. When compared with the Columbia ecotype wild-type, anac050 mutants that lacked function of ANAC050 exhibited Al sensitivity phenotype, while transgenic lines that overexpressed ANAC050 showed an Al-resistant phenotype, indicating the favorable influence of ANAC050 on preserving Al tolerance in plants. Further analysis indicated that anac050 mutants accumulated more Al in roots, implying that ANAC050 may confer a potential operation of an Al exclusion mechanism. Interestingly, anac050 mutants had down-regulated the expression of the genes encoding MULTIDRUG AND TOXIC COMPOUND EXTRUSION (MATE) and AL-ACTIVATED MALATE TRANSPORTER (ALMT1), which were involved in the secretion of citrate and malate, even though there was no evidence of a direct interaction between them, suggesting ANAC050 may mediate the secretion of citrate and malate indirectly. Together with the decreased hemicellulose content, lower Al content was also discovered in root cell walls and hemicelluloses of anac050 mutants, pointing to a potential interaction between ANAC017 and XYLOGLUCAN ENDOTRANSGLUCOSYLASE/HYDROLASE (XTH). Although there was no evidence of a direct interaction between ANAC050 and XTH31, it is worth mentioning that the expression of XTH31, which is essential for xyloglucan modification, was down-regulated in anac050 mutants irrespective of the amount of Al given. In conclusion, our findings showed that ANAC050 contributed to Al resistance by indirect control of the release of organic acids and the accumulation of cell wall hemicelluloses.

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