F-box protein RAE1 regulates the stability of the aluminum-resistance transcription factor STOP1 in Arabidopsis
| Autor: | Qi Xie, Xuan Xu, Fanglin Zhou, Somesh Singh, Jie Zhang, Yang Zhang, Jinliang Guo, Zhongbao Yang, Chao-Feng Huang |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
0106 biological sciences
0301 basic medicine Proteasome Endopeptidase Complex Arabidopsis medicine.disease_cause 01 natural sciences F-box protein 03 medical and health sciences Ubiquitin Gene Expression Regulation Plant medicine Cloning Molecular Transcription factor Gene Regulation of gene expression Mutation Multidisciplinary biology Chemistry Arabidopsis Proteins Ubiquitination biology.organism_classification Cell biology Ubiquitin ligase Nuclear Pore Complex Proteins 030104 developmental biology PNAS Plus biology.protein 010606 plant biology & botany Aluminum Transcription Factors |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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