SUMO E3 ligase AtMMS21-dependent SUMOylation of AUXIN/INDOLE-3-ACETIC ACID 17 regulates auxin signaling
SUMO E3 ligase AtMMS21-dependent SUMOylation of AUXIN/INDOLE-3-ACETIC ACID 17 regulates auxin signaling
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SUMO E3 连接酶 AtMMS21 依赖性 AUXIN/INDOLE-3-ACETIC ACID 17 的 SUMO 化调节生长素信号传导
DOI：
10.1093/plphys/kiac553
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发表时间：
2022
期刊：
影响因子：
7.4
通讯作者：
Chengwei Yang
中科院分区：
文献类型：
--
作者：
Cheng Zhang;Yi Yang;Zhibo Yu;Jun Wang;Ruihua Huang;Qiuna Zhan;Shangze Li;Jianbin Lai;Shengchun Zhang;Chengwei Yang
抽象的。植物生长素水平的变化可以被感知并通过生长素信号转导转化为细胞反应。生长素/吲哚-3-乙酸（Aux/IAA）蛋白是生长素的转录抑制因子，在调节生长素信号转导中起重要作用。Aux/IAA蛋白的稳定性对转录起始和下游生长素相关基因的表达具有重要意义。在这里，我们报告的Aux/IAA蛋白IAA 17相互作用的小泛素相关的修改器（SUMO）E3连接酶甲基甲磺酸敏感21（AtMMS 21）在拟南芥（拟南芥）。AtMMS 21在K41位点调节IAA 17的SUMO化。值得注意的是，根长在过表达IAA 17的植物中受到抑制，而K41突变的IAA 17转基因植物的根与野生型根没有显著差异。生化数据表明，K41突变的IAA 17或AtMMS 21敲除突变体中的IAA 17与野生型植物中的非突变的IAA 17相比更可能被降解。总之，我们的数据揭示了SUMO化在维持IAA 17蛋白稳定性中的作用，这有助于提高我们对生长素信号转导机制的理解。
Abstract. Changes in plant auxin levels can be perceived and converted into cellular responses by auxin signal transduction. AUXIN/INDOLE-3-ACETIC ACID (Aux/IAA) proteins are auxin transcriptional inhibitors that play important roles in regulating auxin signal transduction. The stability of Aux/IAA proteins is important for transcription initiation and downstream auxin-related gene expression. Here, we report that the Aux/IAA protein IAA17 interacts with the small ubiquitin-related modifier (SUMO) E3 ligase METHYL METHANESULFONATE-SENSITIVE 21 (AtMMS21) in Arabidopsis (Arabidopsis thaliana). AtMMS21 regulated the SUMOylation of IAA17 at the K41 site. Notably, root length was suppressed in plants overexpressing IAA17, whereas the roots of K41-mutated IAA17 transgenic plants were not significantly different from wild-type roots. Biochemical data indicated that K41-mutated IAA17 or IAA17 in the AtMMS21 knock-out mutant was more likely to be degraded compared to non-mutated IAA17 in wild-type plants. In conclusion, our data revealed a role for SUMOylation in the maintenance of IAA17 protein stability, which contributes to improving our understanding of the mechanisms of auxin signaling.