Key message

This review summarizes the process of thermal acquired tolerance in plants and the knowledge gap compared to systemic acquired resistance that a plant shows after pathogen inoculation.

Abstract

Plants are continuously challenged by several biotic stresses such as pests and pathogens, or abiotic stresses like high light, UV radiation, drought, salt, and very high or low temperature. Interestingly, for most stresses, prior exposure makes plants more tolerant during the subsequent exposures, which is often referred to as acclimatization. Research of the last two decades reveals that the memory of most of the stresses is associated with epigenetic changes. Heat stress causes damage to membrane proteins, denaturation and inactivation of various enzymes, and accumulation of reactive oxygen species leading to cell injury and death. Plants are equipped with thermosensors that can recognize certain specific changes and activate protection machinery. Phytochrome and calcium signaling play critical roles in sensing sudden changes in temperature and activate cascades of signaling, leading to the production of heat shock proteins (HSPs) that keep protein-unfolding under control. Heat shock factors (HSFs) are the transcription factors that read the activation of thermosensors and induce the expression of HSPs. Epigenetic modifications of HSFs are likely to be the key component of thermal acquired tolerance (TAT). Despite the advances in understanding the process of thermomemory generation, it is not known whether plants are equipped with systemic activation thermal protection, as happens in the form of systemic acquired resistance (SAR) upon pathogen infection. This review describes the recent advances in the understanding of thermomemory development in plants and the knowledge gap in comparison with SAR.

中文翻译：

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植物热记忆的最新进展

关键信息

本综述总结了植物获得热耐受的过程以及与植物在病原体接种后表现出的系统获得性抗性相比的知识差距。

抽象的

植物不断受到多种生物胁迫的挑战，例如害虫和病原体，或非生物胁迫，例如高光、紫外线辐射、干旱、盐分以及极高或极低的温度。有趣的是，对于大多数压力，先前的暴露使植物在随后的暴露期间更具耐受性，这通常被称为驯化。过去二十年的研究表明，大多数压力的记忆与表观遗传变化有关。热应激导致膜蛋白损伤、各种酶的变性和失活以及活性氧的积累导致细胞损伤和死亡。植物配备了热传感器，可以识别某些特定变化并激活保护机制。光敏色素和钙信号在感知温度的突然变化和激活级联信号方面发挥着关键作用，从而导致热休克蛋白 (HSP) 的产生，从而使蛋白质的展开受到控制。热休克因子 (HSFs) 是读取热传感器激活并诱导 HSPs 表达的转录因子。HSF 的表观遗传修饰可能是热获得性耐受 (TAT) 的关键组成部分。尽管在理解热记忆产生过程方面取得了进展，但尚不清楚植物是否配备了系统激活热保护，就像病原体感染后的系统获得性抗性 (SAR) 形式发生的那样。