Zhu Kaijie, Wang Xueke, Sun Jingxian, Noor Iqra, Du Zezheng, Hasanuzzaman Mirza, Wang Chuang, Li Guohuai, Liu Junwei
National Key Laboratory for Germplasm Innovation & Utilisation of Horticultural Crops, College of Horticulture and Forestry Sciences, Huazhong Agricultural University, Wuhan, China.
Microelement Research Center, College of Resources & Environment, Huazhong Agricultural University, Wuhan, China.
Plant Cell Environ. 2025 Jun;48(6):4703-4718. doi: 10.1111/pce.15468. Epub 2025 Mar 11.
Manganese (Mn) toxicity poses a severe hazard to plant growth, with organic acids playing a crucial role in detoxifying toxic metals. However, the regulatory mechanisms governing the response of organic acids to Mn toxicity remain largely elusive, particularly in perennial fruit crops. Herein, we investigated the physio-biochemical and transcriptomic responses of peach seedlings to Mn toxicity. Organic acids, especially malate, significantly increased in Mn-treated peach seedlings. Subsequently, malate application markedly mitigated Mn toxicity in peach. Further, we identified a key vacuolar malate transporter, PpTDT, whose expression was dramatically induced by both Mn and malate treatments. PpTDT was localised to the vacuolar membrane. Heterologous expression of PpTDT in yeast restored growth arrest and enhanced Mn tolerance. Overexpression of PpTDT in tobacco, peach leaves and roots enhanced Mn toxicity tolerance, and increased malate and Mn content. Conversely, silencing of PpTDT in peach seedlings exacerbated Mn toxicity, resulting in decreased malate and Mn content. These findings unveil the role of PpTDT in facilitating intracellular chelation of Mn through malate transport, thereby imparting Mn toxicity tolerance in peach. Our study also highlights the potential of malate as an natural compound for improving Mn toxicity tolerance in peach and potentially other fruit crops.
锰（Mn）毒性对植物生长构成严重危害，有机酸在有毒金属解毒过程中发挥着关键作用。然而，有机酸对锰毒性响应的调控机制仍 largely 难以捉摸，尤其是在多年生果树作物中。在此，我们研究了桃幼苗对锰毒性的生理生化和转录组反应。在锰处理的桃幼苗中，有机酸尤其是苹果酸显著增加。随后，施用苹果酸显著减轻了桃中的锰毒性。此外，我们鉴定出一个关键的液泡苹果酸转运蛋白 PpTDT，其表达受到锰和苹果酸处理的显著诱导。PpTDT 定位于液泡膜。PpTDT 在酵母中的异源表达恢复了生长停滞并增强了锰耐受性。在烟草、桃叶和根中过表达 PpTDT 增强了对锰毒性的耐受性，并增加了苹果酸和锰的含量。相反，桃幼苗中 PpTDT 的沉默加剧了锰毒性，导致苹果酸和锰含量降低。这些发现揭示了 PpTDT 通过苹果酸转运促进细胞内锰螯合从而赋予桃对锰毒性耐受性的作用。我们的研究还强调了苹果酸作为一种天然化合物在提高桃以及潜在其他果树作物对锰毒性耐受性方面的潜力。
