F-box protein RAE1 regulates the stability of the aluminum-resistance transcription factor STOP1 in <i>Arabidopsis</i>.

Abstract

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. <i>Arabidopsis</i>, 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 <i>AtALMT1</i> Here, we identify and characterize an F-box protein-encoding gene <i>regulation of Atalmt1 expression 1</i> (<i>RAE1</i>) that regulates the level of STOP1. Mutation and overexpression of <i>RAE1</i> increases or decreases the expression of <i>AtALMT1</i> 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 <i>RAE1</i> expression by directly binding to the <i>RAE1</i> 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.