F-box protein RAE1 regulates the stability of the aluminum-resistance transcription factor STOP1 in Arabidopsis
F-box protein RAE1 regulates the stability of the aluminum-resistance transcription factor STOP1 in Arabidopsis
复制标题
F-box蛋白RAE1调节拟南芥耐铝转录因子STOP1的稳定性
DOI：
10.1073/pnas.1814426116
复制
发表时间：
2019-01-02
影响因子：
11.1
通讯作者：
Huang, Chao-Feng
中科院分区：
文献类型：
--
作者：
Zhang, Yang;Zhang, Jie;Huang, Chao-Feng
铝毒是酸性土壤上作物生产的主要限制因素。拟南芥可以通过AtALMT 1转运蛋白分泌苹果酸来螯合和解毒铝。转录因子STOP 1是拟南芥抗铝的必需因子，主要通过控制AtALMT 1的表达。在这里，我们报告的F-盒蛋白RAE 1，调节STOP 1的稳定性。RAE 1与STOP 1相互作用，通过泛素-26S蛋白酶体途径促进STOP 1降解，而铝胁迫稳定STOP 1。总之，我们的研究结果揭示了RAE 1在铝抗性调节中的重要作用。铝毒是酸性土壤上限制作物生产的主要因素，酸性土壤占世界可耕地面积的30%以上。一些植物已经进化出了解毒铝的机制。例如，拟南芥通过AtALMT 1转运蛋白分泌苹果酸来螯合和解毒铝。C2 H2型转录因子STOP 1通过诱导一组基因的表达在铝抗性中起着至关重要的作用，包括AtALMT 1。在这里，我们确定和表征的F-box蛋白编码基因调控Atalmt 1表达1（RAE 1），调节STOP 1的水平。RAE 1的突变和过表达分别增加或减少AtALMT 1和其他STOP 1调节基因的表达。RAE 1通过泛素-26S蛋白酶体途径与STOP 1相互作用并促进STOP 1的降解，而铝胁迫促进STOP 1的积累。我们发现STOP 1通过直接结合RAE 1启动子上调RAE 1表达，从而在STOP 1和RAE 1之间形成负反馈环。我们的研究结果表明，RAE 1影响铝抗性通过泛素化和降解的STOP 1。
Significance Aluminum (Al) toxicity is a major constraint of crop production on acid soils. Arabidopsis can secrete malate via the AtALMT1 transporter to chelate and detoxify Al. The transcription factor STOP1 is essentially required for Al resistance, mainly through the control of AtALMT1 expression. Here, we report an F-box protein RAE1 that regulates STOP1 stability. RAE1 interacts with STOP1 to promote STOP1 degradation via the ubiquitin-26S proteasome pathway, whereas Al stress stabilizes STOP1. Together, our results reveal an important role for RAE1 in the regulation of Al resistance. 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.