INRA, Laboratoire des Interactions Plantes-Microorganismes, UMR441, Castanet-Tolosan F-31326, France.
Nat Commun. 2013;4:1476. doi: 10.1038/ncomms2479.
One of the most efficient plant resistance reactions to pathogen attack is the hypersensitive response, a form of programmed cell death at infection sites. The Arabidopsis transcription factor MYB30 is a positive regulator of hypersensitive cell death responses. Here we show that MIEL1 (MYB30-Interacting E3 Ligase1), an Arabidopsis RING-type E3 ubiquitin ligase that interacts with and ubiquitinates MYB30, leads to MYB30 proteasomal degradation and downregulation of its transcriptional activity. In non-infected plants, MIEL1 attenuates cell death and defence through degradation of MYB30. Following bacterial inoculation, repression of MIEL1 expression removes this negative regulation allowing sufficient MYB30 accumulation in the inoculated zone to trigger the hypersensitive response and restrict pathogen growth. Our work underlines the important role played by ubiquitination to control the hypersensitive response and highlights the sophisticated fine-tuning of plant responses to pathogen attack. Overall, this work emphasizes the importance of protein modification by ubiquitination during the regulation of transcriptional responses to stress in eukaryotic cells.
植物对病原体攻击的最有效防御反应之一是过敏反应，这是感染部位程序性细胞死亡的一种形式。拟南芥转录因子 MYB30 是过敏细胞死亡反应的正调节剂。在这里，我们表明，MIEL1（MYB30 相互作用的 E3 连接酶 1），一种与 MYB30 相互作用并泛素化 MYB30 的拟南芥 RING 型 E3 泛素连接酶，导致 MYB30 蛋白酶体降解和转录活性下调。在未感染的植物中，MIEL1 通过降解 MYB30 来减弱细胞死亡和防御。在细菌接种后，抑制 MIEL1 的表达会消除这种负调控，从而使接种区有足够的 MYB30 积累来触发过敏反应并限制病原体生长。我们的工作强调了泛素化在控制过敏反应中的重要作用，并突出了植物对病原体攻击的反应的精细调控。总的来说，这项工作强调了在真核细胞中，蛋白质修饰通过泛素化在调节转录反应对压力的反应中的重要性。
