植物免疫:处于病原体感知和防御反应的十字路口

Plants Pub Date : 2024-05-22 DOI:10.3390/plants13111434
S. Ali, A. Tyagi, Z. Mir
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摘要

植物会受到不同微生物病原体的挑战,从而影响其生长和产量。然而,为了抵御病原体的侵袭,植物会使用多种免疫反应,如模式触发免疫(PTI)、效应触发免疫(ETI)、RNA 沉默和自噬等,这些免疫反应错综复杂,并受到不同信号级联的调控。模式识别受体(PRR)和核苷酸结合富亮氨酸重复(NLR)受体是植物先天免疫的标志,因为它们能检测病原体或相关免疫原性信号,并在不同细胞区触发一系列免疫信号级联。在植物中,最常见的 PRRs 是类受体激酶(RLKs)和类受体蛋白(RLPs),它们起着第一层诱导性防御的作用。在本综述中,我们将介绍植物如何感知作为危险信号的病原体、微生物相关分子模式(PAMPs 或 MAMPs)和效应物,并激活不同的免疫反应,如 PTI 和 ETI。此外,我们还讨论了 RNA 沉默、自噬和系统获得性抗性作为宿主对病原体的多功能防御反应的作用。我们还讨论了引发不同植物免疫反应激活的早期生化信号事件,如钙(Ca2+)、活性氧(ROS)和激素。本综述还强调了气候驱动的环境因素对宿主与病原体相互作用的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Plant Immunity: At the Crossroads of Pathogen Perception and Defense Response
Plants are challenged by different microbial pathogens that affect their growth and productivity. However, to defend pathogen attack, plants use diverse immune responses, such as pattern-triggered immunity (PTI), effector-triggered immunity (ETI), RNA silencing and autophagy, which are intricate and regulated by diverse signaling cascades. Pattern-recognition receptors (PRRs) and nucleotide-binding leucine-rich repeat (NLR) receptors are the hallmarks of plant innate immunity because they can detect pathogen or related immunogenic signals and trigger series of immune signaling cascades at different cellular compartments. In plants, most commonly, PRRs are receptor-like kinases (RLKs) and receptor-like proteins (RLPs) that function as a first layer of inducible defense. In this review, we provide an update on how plants sense pathogens, microbe-associated molecular patterns (PAMPs or MAMPs), and effectors as a danger signals and activate different immune responses like PTI and ETI. Further, we discuss the role RNA silencing, autophagy, and systemic acquired resistance as a versatile host defense response against pathogens. We also discuss early biochemical signaling events such as calcium (Ca2+), reactive oxygen species (ROS), and hormones that trigger the activation of different plant immune responses. This review also highlights the impact of climate-driven environmental factors on host–pathogen interactions.
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