期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 116, 期 1, 页码 319-327出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1814426116
关键词
aluminum toxicity; AtALMT1; E3 ligase; low phosphate response; ubiquitination
资金
- National Natural Science Foundation of China [31570253]
- Jiangsu Science Fund for Distinguished Young Scholars [BK20150027]
- Strategic Priority Research Program of the Chinese Academy of Sciences [XDB27040000]
- Shanghai Center for Plant Stress Biology, 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 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-265 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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