Shanghai Center for Plant Stress Biology and National Key Laboratory of Plant Molecular Genetics, Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences, Shanghai 200032, China.
State Key Laboratory of Crop Genetics and Germplasm Enhancement, College of Resources and Environmental Sciences, Nanjing Agricultural University, Nanjing 210095, China.
Plant Cell. 2020 Dec;32(12):3921-3938. doi: 10.1105/tpc.20.00687. Epub 2020 Oct 21.
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 () 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 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 increases the level of STOP1 SUMOylation and the expression of the STOP1-regulated gene , which contributes to the increased Al resistance in The mutation does not influence STOP1 protein abundance but increases the association of STOP1 with the promoter, which might explain the elevated expression of in 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.
铝（Al）是酸性土壤作物生产的主要限制因素，酸性土壤占世界可耕地的 30%以上。拟南芥中的铝抗性是通过 Al-ACTIVATED MALATE TRANSPORTER1（AtALMT1）转运蛋白介导的苹果酸分泌来实现的。C2H2 型转录因子 SENSITIVE TO PROTON RHIZOTOXICITY1（STOP1）是必需的，也是铝抗性所必需的，它通过诱导包括在内的铝抗性基因的表达来发挥作用。在这项研究中，我们报告称 STOP1 蛋白功能被 SUMOylation 修饰。SMALL UBIQUITIN-LIKE MODIFIER（SUMO）蛋白酶 ESD4 特异性地与 STOP1 相互作用并去 SUMOylation，但不是其他 SUMO 蛋白酶。突变增加了 STOP1 SUMOylation的水平和 STOP1 调节基因的表达，这有助于提高突变体中的铝抗性。突变不影响 STOP1 蛋白丰度，但增加了 STOP1 与启动子的结合，这可能解释了在突变体中基因的表达升高。我们证明 STOP1 在 K40、K212 或 K395 位点被单 SUMO 化，并且阻断 STOP1 SUMOylation 会降低 STOP1 的稳定性和 STOP1 调节基因的表达，从而降低铝抗性。因此，我们的结果揭示了 SUMOylation 在拟南芥 STOP1 调节和铝抗性中的参与。
