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      Stress priming, memory, and signalling in plants : Stress priming, memory, and signalling in plants

      1 , 2
      Plant, Cell & Environment
      Wiley

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          Abstract

          Plants need to cope with changing environmental conditions, be it variable light or temperature, different availability of water or nutrients, or attack by pathogens or insects. Some of these changing conditions can become stressful and require strong countermeasures to ensure plant survival. Plants have evolved numerous distinct sensing and signalling mechanisms to perceive and respond appropriately to a variety of stresses. Because of the unpredictable nature of numerous stresses, resource-saving stress response mechanisms are inducible and become activated only upon a stress experience. Furthermore, plants have evolved mechanisms by which they can remember past stress events and prime their responses in order to react more rapidly or more strongly to recurrent stress. Research over the last decade has revealed mechanisms of this information storage and retrieval, which include epigenetic regulation, transcriptional priming, primed conformation of proteins, or specific hormonal or metabolic signatures. There is also increasing understanding of the ecological constraints and relevance of stress priming and memory. This special issue presents research articles and reviews addressing various aspects of this exciting and growing field of research. Here, we introduce the topic by referring to the articles published in this issue, and we outline open questions and future directions of research.

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          Most cited references72

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          Induced systemic resistance by beneficial microbes.

          Beneficial microbes in the microbiome of plant roots improve plant health. Induced systemic resistance (ISR) emerged as an important mechanism by which selected plant growth-promoting bacteria and fungi in the rhizosphere prime the whole plant body for enhanced defense against a broad range of pathogens and insect herbivores. A wide variety of root-associated mutualists, including Pseudomonas, Bacillus, Trichoderma, and mycorrhiza species sensitize the plant immune system for enhanced defense without directly activating costly defenses. This review focuses on molecular processes at the interface between plant roots and ISR-eliciting mutualists, and on the progress in our understanding of ISR signaling and systemic defense priming. The central role of the root-specific transcription factor MYB72 in the onset of ISR and the role of phytohormones and defense regulatory proteins in the expression of ISR in aboveground plant parts are highlighted. Finally, the ecological function of ISR-inducing microbes in the root microbiome is discussed.
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            Growth-defense tradeoffs in plants: a balancing act to optimize fitness.

            Growth-defense tradeoffs are thought to occur in plants due to resource restrictions, which demand prioritization towards either growth or defense, depending on external and internal factors. These tradeoffs have profound implications in agriculture and natural ecosystems, as both processes are vital for plant survival, reproduction, and, ultimately, plant fitness. While many of the molecular mechanisms underlying growth and defense tradeoffs remain to be elucidated, hormone crosstalk has emerged as a major player in regulating tradeoffs needed to achieve a balance. In this review, we cover recent advances in understanding growth-defense tradeoffs in plants as well as what is known regarding the underlying molecular mechanisms. Specifically, we address evidence supporting the growth-defense tradeoff concept, as well as known interactions between defense signaling and growth signaling. Understanding the molecular basis of these tradeoffs in plants should provide a foundation for the development of breeding strategies that optimize the growth-defense balance to maximize crop yield to meet rising global food and biofuel demands. © The Author 2014. Published by the Molecular Plant Shanghai Editorial Office in association with Oxford University Press on behalf of CSPB and IPPE, SIBS, CAS.
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              Systemic acquired resistance: turning local infection into global defense.

              Systemic acquired resistance (SAR) is an induced immune mechanism in plants. Unlike vertebrate adaptive immunity, SAR is broad spectrum, with no specificity to the initial infection. An avirulent pathogen causing local programmed cell death can induce SAR through generation of mobile signals, accumulation of the defense hormone salicylic acid, and secretion of the antimicrobial PR (pathogenesis-related) proteins. Consequently, the rest of the plant is protected from secondary infection for a period of weeks to months. SAR can even be passed on to progeny through epigenetic regulation. The Arabidopsis NPR1 (nonexpresser of PR genes 1) protein is a master regulator of SAR. Recent study has shown that salicylic acid directly binds to the NPR1 adaptor proteins NPR3 and NPR4, regulates their interactions with NPR1, and controls NPR1 protein stability. However, how NPR1 interacts with TGA transcription factors to activate defense gene expression is still not well understood. In addition, redox regulators, the mediator complex, WRKY transcription factors, endoplasmic reticulum-resident proteins, and DNA repair proteins play critical roles in SAR.
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                Author and article information

                Journal
                Plant, Cell & Environment
                Plant Cell Environ
                Wiley
                01407791
                March 2019
                March 2019
                February 19 2019
                : 42
                : 3
                : 753-761
                Affiliations
                [1 ]Dahlem Centre of Plant Sciences (DCPS), Institute of Biology/Applied Zoology & Ecology; Freie Universität Berlin; D-14163 Berlin Germany
                [2 ]Dahlem Centre of Plant Sciences (DCPS), Institute of Biology/Applied Genetics; Freie Universität Berlin; D-14195 Berlin Germany
                Article
                10.1111/pce.13526
                30779228
                ea520058-4852-44f3-bf78-27c091b035f4
                © 2019

                http://doi.wiley.com/10.1002/tdm_license_1.1

                http://onlinelibrary.wiley.com/termsAndConditions#vor

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