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Arabidopsis ubiquitin ligase MIEL1 mediatesdegradation of the transcription factorMYB30 weakening plant defence

机译:拟南芥泛素连接酶MIEL1介导转录因子MYB30的降解,削弱植物防御能力

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One of the most efficient plant resistance reactions to pathogen attack is the hypersensitiveresponse, a form of programmed cell death at infection sites. The Arabidopsis transcriptionfactor MYB30 is a positive regulator of hypersensitive cell death responses. Here we showthat MIEL1 (MYB30-Interacting E3 Ligase1), an Arabidopsis RING-type E3 ubiquitin ligasethat interacts with and ubiquitinates MYB30, leads to MYB30 proteasomal degradation anddownregulation of its transcriptional activity. In non-infected plants, MIEL1 attenuates celldeath and defence through degradation of MYB30. Following bacterial inoculation, repressionof MIEL1 expression removes this negative regulation allowing sufficient MYB30 accumulationin the inoculated zone to trigger the hypersensitive response and restrict pathogengrowth. Our work underlines the important role played by ubiquitination to control thehypersensitive response and highlights the sophisticated fine-tuning of plant responses topathogen attack. Overall, this work emphasizes the importance of protein modification byubiquitination during the regulation of transcriptional responses to stress in eukaryotic cells.
机译:对病原体侵袭最有效的植物抗性反应之一是超敏反应,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是超敏细胞死亡反应的正向调节剂。在这里,我们显示MIEL1(与MYB30相互作用的E3连接酶1)是一种拟南芥RING型E3泛素连接酶,可与MYB30相互作用并使其泛素化,从而导致MYB30蛋白酶体降解和其转录活性下调。在未感染的植物中,MIEL1通过降解MYB30减弱细胞死亡和防御能力。细菌接种后,MIEL1表达的抑制消除了这种负调控,使MYB30在接种区中积累足够,从而触发超敏反应并限制病原体的生长。我们的工作强调了泛素化在控制过敏反应中所起的重要作用,并强调了植物对病原体侵袭的精细调节。总的来说,这项工作强调了在调控真核细胞对应激的转录反应过程中,泛素化修饰蛋白质的重要​​性。

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