Herbivore attack elicits costly defenses that are known to decrease plant fitness by using resources that are normally slated for growth and reproduction. Additionally, plants have evolved mechanisms for tolerating attack, which are not understood on a molecular level. Using 11 C-photosynthate labeling as well as sugar and enzyme measurements, we found rapid changes in sink-source relations in the annual Nicotiana attenuata after simulated herbivore attacks, which increased the allocation of sugars to roots. This herbivore-induced response is regulated by the -subunit of an SnRK1 (SNF1-related kinase) protein kinase, GAL83, transcripts of which are rapidly down-regulated in source leaves after herbivore attack and, when silenced, increase assimilate transport to roots. This C diversion response is activated by herbivore-specific elicitors and is independent of jasmonate signaling, which regulates most of the plant's defense responses. Herbivore attack during early stages of development increases root reserves, which, in turn, delays senescence and prolongs flowering. That attacked GAL83-silenced plants use their enhanced root reserves to prolong reproduction demonstrates that SnRK1 alters resource allocation so that plants better tolerate herbivory. This tolerance mechanism complements the likely defensive value of diverting resources to a less vulnerable location within the plant.carbon-11 ͉ defense ͉ plant-herbivore interactions ͉ tolerance P lants have evolved a variety of mechanisms for reducing the negative impact of herbivore attack on fitness; these mechanisms include direct and indirect defenses and tolerance (1). Defenses are costly, expending energy and resources that could otherwise be used to grow and generate offspring. Inducible defenses allow plants to invest resources into defense only when needed. Although defenses limit the extent of damage, even well defended plants lose large amounts of tissue when attacked by herbivores that have adapted to their defenses. Then, plants would benefit from tolerance, which minimizes the fitness consequences of tissue loss to herbivores (2-4). Defense against, and tolerance of, herbivory are not mutually exclusive; most plantinsect interactions likely combine both (5, 6). In contrast to the rapid advances in our understanding of defense mechanisms, little is known about the traits that allow plants to tolerate herbivore damage.Tolerance, which is measured by comparing the fitness of a genotype in environments with and without attackers, remains uncharacterized at the molecular level (2, 7). At a physiological level, increases in photosynthetic rate, branching, and storage in belowground tissues are thought to be involved (8-10). These responses require the tuning of primary metabolism, for which mutant screens and other reverse genetic approaches with model plants have yet to yield molecular regulators. Host plants that have coevolved with adapted herbivores likely have elaborate defense and tolerance responses to minimize the fitness consequences of herbivory...
Experience and memory of environmental stimuli that indicate future stress can prepare (prime) organismic stress responses even in species lacking a nervous system. The process through which such organisms prepare their phenotype for an improved response to future stress has been termed 'priming'. However, other terms are also used for this phenomenon, especially when considering priming in different types of organisms and when referring to different stressors. Here we propose a conceptual framework for priming of stress responses in bacteria, fungi and plants which allows comparison of priming with other terms, e.g. adaptation, acclimation, induction, acquired resistance and cross protection. We address spatial and temporal aspects of priming and highlight current knowledge about the mechanisms necessary for information storage which range from epigenetic marks to the accumulation of (dormant) signalling molecules. Furthermore, we outline possible patterns of primed stress responses. Finally, we link the ability of organisms to become primed for stress responses (their 'primability') with evolutionary ecology aspects and discuss which properties of an organism and its environment may favour the evolution of priming of stress responses.
Plants evolved mechanisms to counteract bacterial infection by preparing yet uninfected systemic tissues for an enhanced defense response, so-called systemic acquired resistance or priming responses. Primed leaves express a wide range of genes that enhance the defense response once an infection takes place. While hormone-driven defense signalling and defensive metabolites have been well studied, less focus has been set on the reorganization of primary metabolism in systemic leaves. Since primary metabolism plays an essential role during defense to provide energy and chemical building blocks, we investigated changes in primary metabolism at RNA and metabolite levels in systemic leaves of Arabidopsis thaliana plants that were locally infected with Pseudomonas syringae. Known defense genes were still activated 3–4 days after infection. Also primary metabolism was significantly altered. Nitrogen (N)-metabolism and content of amino acids and other N-containing metabolites were significantly reduced, whereas the organic acids fumarate and malate were strongly increased. We suggest that reduction of N-metabolites in systemic leaves primes defense against bacterial infection by reducing the nutritional value of systemic tissue. Increased organic acids serve as quickly available metabolic resources of energy and carbon-building blocks for the production of defense metabolites during subsequent secondary infections.
Metabolism is the system layer that determines growth by the rate of matter uptake and conversion into biomass. The scaffold of enzymatic reaction rates drives the metabolic network in a given physico-chemical environment. In response to the diverse environmental stresses, plants have evolved the capability of integrating macro- and micro-environmental events to be prepared, i.e., to be primed for upcoming environmental challenges. The hierarchical view on stress signaling, where metabolites are seen as final downstream products, has recently been complemented by findings that metabolites themselves function as stress signals. We present a systematic concept of metabolic responses that are induced by environmental stresses and persist in the plant system. Such metabolic imprints may prime metabolic responses of plants for subsequent environmental stresses. We describe response types with examples of biotic and abiotic environmental stresses and suggest that plants use metabolic imprints, the metabolic changes that last beyond recovery from stress events, and priming, the imprints that function to prepare for upcoming stresses, to integrate diverse environmental stress histories. As a consequence, even genetically identical plants should be studied and understood as phenotypically plastic organisms that continuously adjust their metabolic state in response to their individually experienced local environment. To explore the occurrence and to unravel functions of metabolic imprints, we encourage researchers to extend stress studies by including detailed metabolic and stress response monitoring into extended recovery phases.
This book chapter describes the analytical procedures required for the profiling of a metabolite fraction enriched for primary metabolites. The profiling is based on routine gas chromatography coupled to mass spectrometry (GC-MS). The generic profiling method is adapted to plant material, specifically to the analysis of single leaves from plants that were exposed to temperature stress experiments. The described method is modular. The modules include a rapid sampling and metabolic inactivation protocol for samples in a wide size range, a sample extraction procedure, a chemical derivatization step that is required to make the metabolite fraction amenable to gas chromatographic analysis, a routine GC-MS method, and finally the procedures of data processing and data mining. A basic and extendable set of standardizations for metabolite recovery and retention index alignment of the resulting GC-MS chromatograms is included. The method has two applications: (1) the rapid screening for changes of relative metabolite pools sizes under temperature stress and (2) the verification of cold-regulated metabolites by exact quantification using a GC-MS protocol with extended internal and external standardization.
Exposure to smoke is required for the germination of seeds from dormant genotypes of Nicotiana attenuata, a post-fire annual of the Great Basin Desert. Germination can be elicited by GA(1,3,4,7) treatments and inhibited by the GA biosynthesis inhibitor
Plant diseases caused by pathogenic bacteria or fungi cause major economic damage every year and destroy crop yields that could feed millions of people. Only by a thorough understanding of the interaction between plants and phytopathogens can we hope to develop strategies to avoid or treat the outbreak of large-scale crop pests. Here, we studied the interaction of plant-pathogen pairs at the metabolic level. We selected five plant-pathogen pairs, for which both genomes were fully sequenced, and constructed the corresponding genome-scale metabolic networks. We present theoretical investigations of the metabolic interactions and quantify the positive and negative effects a network has on the other when combined into a single plant-pathogen pair network. Merged networks were examined for both the native plant-pathogen pairs as well as all other combinations. Our calculations indicate that the presence of the parasite metabolic networks reduce the ability of the plants to synthesize key biomass precursors. While the producibility of some precursors is reduced in all investigated pairs, others are only impaired in specific plant-pathogen pairs. Interestingly, we found that the specific effects on the host’s metabolism are largely dictated by the pathogen and not by the host plant. We provide graphical network maps for the native plant-pathogen pairs to allow for an interactive interrogation. By exemplifying a systematic reconstruction of metabolic network pairs for five pathogen-host pairs and by outlining various theoretical approaches to study the interaction of plants and phytopathogens on a biochemical level, we demonstrate the potential of investigating pathogen-host interactions from the perspective of interacting metabolic networks that will contribute to furthering our understanding of mechanisms underlying a successful invasion and subsequent establishment of a parasite into a plant host.
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