National Key Laboratory of Plant Molecular Genetics, Shanghai Center for Plant Stress Biology, Center of Excellence for Molecular Plant Sciences, Chinese Academy of Sciences, 200032 Shanghai, China.
College of Resources and Environmental Sciences, Nanjing Agricultural University, 210095 Nanjing, China.
Proc Natl Acad Sci U S A. 2019 Jan 2;116(1):319-327. doi: 10.1073/pnas.1814426116. Epub 2018 Dec 17.
Aluminum (Al) toxicity is a major factor limiting crop production on acid soils, which represent over 30% of the world's arable land. Some plants have evolved mechanisms to detoxify Al. , for example, secretes malate via the AtALMT1 transporter to chelate and detoxify Al. The C2H2-type transcription factor STOP1 plays a crucial role in Al resistance by inducing the expression of a set of genes, including Here, we identify and characterize an F-box protein-encoding gene () that regulates the level of STOP1. Mutation and overexpression of increases or decreases the expression of and other STOP1-regulated genes, respectively. RAE1 interacts with and promotes the degradation of STOP1 via the ubiquitin-26S proteasome pathway, while Al stress promotes the accumulation of STOP1. We find that STOP1 up-regulates expression by directly binding to the promoter, thus forming a negative feedback loop between STOP1 and RAE1. Our results demonstrate that RAE1 influences Al resistance through the ubiquitination and degradation of STOP1.
铝(Al)毒性是限制酸性土壤上作物生产的主要因素,酸性土壤占世界可耕地的 30%以上。一些植物已经进化出了解毒 Al 的机制。例如,通过 AtALMT1 转运蛋白分泌苹果酸来螯合和解毒 Al。C2H2 型转录因子 STOP1 通过诱导一组基因的表达,包括 ,在 Al 抗性中发挥关键作用。在这里,我们鉴定并表征了一个编码 F-box 蛋白的基因 (),它调节 STOP1 的水平。突变和过表达 分别增加或减少 的表达和其他由 STOP1 调节的基因的表达。RAE1 通过泛素-26S 蛋白酶体途径与 STOP1 相互作用并促进其降解,而 Al 胁迫促进 STOP1 的积累。我们发现 STOP1 通过直接结合 启动子来上调 的表达,从而在 STOP1 和 RAE1 之间形成负反馈环。我们的结果表明,RAE1 通过泛素化和降解 STOP1 来影响 Al 抗性。