Regulation of Aluminum Resistance in Arabidopsis Involves the SUMOylation of the Zinc Finger Transcription Factor STOP1
Regulation of Aluminum Resistance in Arabidopsis Involves the SUMOylation of the Zinc Finger Transcription Factor STOP1
复制标题
拟南芥铝抗性的调节涉及锌指转录因子 STOP1 的 SUMO 化
DOI：
10.1105/tpc.20.00687
复制
发表时间：
2020-12-01
期刊：
影响因子：
11.6
通讯作者：
Huang, Chao-Feng
中科院分区：
文献类型：
--
作者：
Fang, Qiu;Zhang, Jie;Huang, Chao-Feng
铝抗性转录因子STOP 1在K40、K212或K395位点被单SUMO化，并被SUMO蛋白酶ESD 4去SUMO化，ESD 4参与拟南芥铝抗性的调控。在占世界耕地面积30%以上的酸性土壤上，铝是作物生产的主要限制因素。拟南芥（Arabidopsis thaliana）中的铝抗性是通过铝激活的苹果酸转运蛋白1（AtALMT1）介导的苹果酸分泌来实现的。C2H2型转录因子对质子根毒性敏感1（STOP 1）是铝抗性所必需的，它通过诱导包括AtALMT 1在内的铝抗性基因的表达而起作用。在这项研究中，我们报告STOP 1蛋白功能通过SUMO化修饰。小泛素样修饰物（SUMO）蛋白酶ESD4，而不是其他SUMO蛋白酶，特异性地与STOP1相互作用并使其去SUMO化。ESD4的突变增加了STOP1 SUMO化的水平和STOP1调节基因AtALMT1的表达，这有助于提高esd4的铝抗性。esd 4突变不影响STOP 1蛋白丰度，但增加了STOP 1与AtALMT 1启动子的关联，这可能解释了AtALMT 1在esd 4中的表达升高。我们证明了STOP1在K40、K212或K395位点被单SUMO化，阻断STOP1 SUMO化降低了STOP1的稳定性和STOP1调控基因的表达，导致铝抗性降低。因此，我们的研究结果揭示了SUMO化参与调控拟南芥的STOP1和铝抗性。
The Al-resistance transcription factor STOP1 is mono-SUMOylated at K40, K212, or K395 sites and deSUMOylated by the SUMO protease ESD4, which is involved in the regulation of Al resistance in Arabidopsis. Aluminum (Al) is a primary constraint for crop production on acid soils, which make up more than 30% of the arable land in the world. Al resistance in Arabidopsis (Arabidopsis thaliana) is achieved by malate secretion mediated by the Al-ACTIVATED MALATE TRANSPORTER1 (AtALMT1) transporter. The C2H2-type transcription factor SENSITIVE TO PROTON RHIZOTOXICITY1 (STOP1) is essential and required for Al resistance, where it acts by inducing the expression of Al-resistance genes, including AtALMT1. In this study, we report that STOP1 protein function is modified by SUMOylation. The SMALL UBIQUITIN-LIKE MODIFIER (SUMO) protease ESD4, but not other SUMO proteases, specifically interacts with and deSUMOylates STOP1. Mutation of ESD4 increases the level of STOP1 SUMOylation and the expression of the STOP1-regulated gene AtALMT1, which contributes to the increased Al resistance in esd4. The esd4 mutation does not influence STOP1 protein abundance but increases the association of STOP1 with the AtALMT1 promoter, which might explain the elevated expression of AtALMT1 in esd4. We demonstrate that STOP1 is mono-SUMOylated at K40, K212, or K395 sites, and blocking STOP1 SUMOylation reduces STOP1 stability and the expression of STOP1-regulated genes, leading to the reduced Al resistance. Our results thus reveal the involvement of SUMOylation in the regulation of STOP1 and Al resistance in Arabidopsis.