期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2019
卷号：116
期号：1
页码：319-327
DOI：10.1073/pnas.1814426116
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：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 regulation of Atalmt1 expression 1 ( RAE1 ) 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 up-regulates 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.
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