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Arabidopsis Proline Dehydrogenase Contributes to Flagellin-Mediated PAMP-Triggered Immunity by Affecting RBOHD

机译:拟南芥脯氨酸脱氢酶通过影响RBOHD促进鞭毛蛋白介导的PAMP触发的免疫

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摘要

Plants activate different defense systems to counteract the attack of microbial pathogens. Among them, the recognition of conserved microbial- or pathogen-associated molecular patterns (MAMPs or PAMPs) by pattern -recognition receptors stimulates MAMP- or PAMP-triggered immunity (PTI). In recent years, the elicitors, receptors, and signaling pathways leading to PTI have been extensively studied. However, the contribution of organelles to this program deserves further characterization. Here, we studied how processes altering the mitochondrial electron transport chain (mETC) influence PTI establishment. With particular emphasis, we evaluated the effect of proline dehydrogenase (ProDH), an enzyme that can load electrons into the mETC and regulate the cellular redox state. We found that mETC uncouplers (antimycin or rotenone) and manganese superoxide dismutase deficiency impair flg22-induced responses such as accumulation of reactive oxygen species (ROS) and bacterial growth limitation. ProDH mutants also reduce these defenses, decreasing callose deposition as well. Using ProDH inhibitors and ProDH inducers (exogenous Pro treatment), we showed that this enzyme modulates the generation of ROS by the plasma membrane respiratory burst NADPH oxidase homolog D. In this way, we contribute to the understanding of mitochondrial activities influencing early and late PTI responses and the coordination of the redox-associated mitochondrial enzyme ProDH with defense events initiated at the plasma membrane.
机译:植物激活不同的防御系统以抵消微生物病原体的攻击。其中,通过模式识别受体识别保守的微生物或病原体相关分子模式(MAMP或PAMP)会刺激MAMP或PAMP触发的免疫(PTI)。近年来,导致PTI的激发子,受体和信号通路已得到广泛研究。但是,细胞器对该程序的贡献值得进一步表征。在这里,我们研究了改变线粒体电子传输链(mETC)的过程如何影响PTI的建立。我们特别强调了脯氨酸脱氢酶(ProDH)的作用,脯氨酸脱氢酶可以将电子加载到mETC中并调节细胞的氧化还原状态。我们发现,mETC解偶联剂(抗霉素或鱼藤酮)和锰超氧化物歧化酶缺陷会削弱flg22诱导的反应,例如活性氧(ROS)的积累和细菌的生长限制。 ProDH突变体也减少了这些防御,也减少了call的沉积。使用ProDH抑制剂和ProDH诱导剂(外源性Pro治疗),我们表明该酶通过质膜呼吸爆发NADPH氧化酶同源物D调节ROS的生成。通过这种方式,我们有助于了解影响早期和晚期PTI的线粒体活性氧化还原相关的线粒体酶ProDH的应答和协调与质膜上引发的防御事件。

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