Chao-Feng Huang / Center of Excellence in Molecular Plant Sciences, Chinese Academy of Sciences
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. Arabidopsis, 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 AtALMT1. Here, we identify and characterize an F-box protein-encoding gene RAE1 (Regulation of AtALMT1 Expression 1) that regulates the level of STOP1. Mutation and overexpression of RAE1 increases or decreases the expression of AtALMT1 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 upregulates RAE1 expression by directly binding to the RAE1 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.