Sweating treatment enhances citrus fruit disease resistance by inducing the accumulation of amino acids and salicylic acid-induced resistance pathway

High-temperature treatment induces disease resistance in various plants (heat shock-induced resistance; HSIR). The role of heat shock transcriptional factors (Hsfs) was investigated in this paper. Heat shock treatment induced disease resistance and up-regulate gene expression of pathogenesis related protein; PR1a2 at 12 and 24 h after treatment. PR1a2 has putative Hsfs binding site in the upstream area. On the other hand, a heat shock transcription factor HsfA2 up-regulated at 6 h after treatment, which was 6 h earlier than salicylic acid accumulation. This time lag suggested the direct contribution of Hsfs, additionally to salicylic acid pathway in the regulation of HSIR in tomato.

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Nanogram Amounts of Salicylic Acid Produced by the Rhizobacterium Pseudomonas aeruginosa 7NSK2 Activate the Systemic Acquired Resistance Pathway in Bean

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi.1999.12.5.450 ◽

1999 ◽

Vol 12 (5) ◽

pp. 450-458 ◽

Cited By ~ 151

Author(s):

Geert De Meyer ◽

Kristof Capieau ◽

Kris Audenaert ◽

Antony Buchala ◽

Jean-Pierre Métraux ◽

...

Keyword(s):

Pseudomonas Aeruginosa ◽

Salicylic Acid ◽

Induced Resistance ◽

Phenylalanine Ammonia Lyase ◽

Systemic Acquired Resistance ◽

Acquired Resistance ◽

Systemic Resistance ◽

Resistance Pathway ◽

Lyase Activity ◽

Phenylalanine Ammonia Lyase Activity

Root colonization by specific nonpathogenic bacteria can induce a systemic resistance in plants to pathogen infections. In bean, this kind of systemic resistance can be induced by the rhizobacterium Pseudomonas aeruginosa 7NSK2 and depends on the production of salicylic acid by this strain. In a model with plants grown in perlite we demonstrated that Pseudomonas aeruginosa 7NSK2-induced resistance is equivalent to the inclusion of 1 nM salicylic acid in the nutrient solution and used the latter treatment to analyze the molecular basis of this phenomenon. Hydroponic feeding of 1 nM salicylic acid solutions induced phenylalanine ammonia-lyase activity in roots and increased free salicylic acid levels in leaves. Because pathogen-induced systemic acquired resistance involves similar changes it was concluded that 7NSK2-induced resistance is mediated by the systemic acquired resistance pathway. This conclusion was validated by analysis of phenylalanine ammonia-lyase activity in roots and of salicylic acid levels in leaves of soil-grown plants treated with Pseudomonas aeruginosa. The induction of systemic acquired resistance by nanogram amounts of salicylic acid is discussed with respect to long-distance signaling in systemic acquired resistance.

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Effects of salicylic acid on disease resistance and postharvest decay control of fruits

Stewart Postharvest Review ◽

10.2212/spr.2007.6.2 ◽

2007 ◽

Vol 3 (6) ◽

pp. 1-7 ◽

Cited By ~ 16

Keyword(s):

Salicylic Acid ◽

Disease Resistance ◽

Postharvest Decay

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Uncoupling Salicylic Acid-Dependent Cell Death and Defense-Related Responses From Disease Resistance in the Arabidopsis Mutant acd5

Genetics ◽

10.1093/genetics/156.1.341 ◽

2000 ◽

Vol 156 (1) ◽

pp. 341-350

Author(s):

Jean T Greenberg ◽

F Paul Silverman ◽

Hua Liang

Keyword(s):

Cell Death ◽

Salicylic Acid ◽

Disease Resistance ◽

Pseudomonas Syringae ◽

Higher Plants ◽

Ethylene Signaling ◽

Symptom Development ◽

Wild Type ◽

Dependent Cell ◽

Arabidopsis Mutant

Abstract Salicylic acid (SA) is required for resistance to many diseases in higher plants. SA-dependent cell death and defense-related responses have been correlated with disease resistance. The accelerated cell death 5 mutant of Arabidopsis provides additional genetic evidence that SA regulates cell death and defense-related responses. However, in acd5, these events are uncoupled from disease resistance. acd5 plants are more susceptible to Pseudomonas syringae early in development and show spontaneous SA accumulation, cell death, and defense-related markers later in development. In acd5 plants, cell death and defense-related responses are SA dependent but they do not confer disease resistance. Double mutants with acd5 and nonexpressor of PR1, in which SA signaling is partially blocked, show greatly attenuated cell death, indicating a role for NPR1 in controlling cell death. The hormone ethylene potentiates the effects of SA and is important for disease symptom development in Arabidopsis. Double mutants of acd5 and ethylene insensitive 2, in which ethylene signaling is blocked, show decreased cell death, supporting a role for ethylene in cell death control. We propose that acd5 plants mimic P. syringae-infected wild-type plants and that both SA and ethylene are normally involved in regulating cell death during some susceptible pathogen infections.

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Paper-containing 1-methylcyclopropene treatment suppresses fruit decay of fresh Anxi persimmons by enhancing disease resistance

Food Quality and Safety ◽

10.1093/fqsafe/fyab007 ◽

2021 ◽

Vol 5 ◽

Author(s):

Lingzhen Zeng ◽

Lili Shi ◽

Hetong Lin ◽

Yuzhao Lin ◽

Yixiong Lin ◽

...

Keyword(s):

Disease Resistance ◽

Decay Rate ◽

Potential Application ◽

Total Phenolics ◽

Lignin Content ◽

Related Substances ◽

Postharvest Treatment ◽

Cent Relative Humidity ◽

Fruit Decay ◽

Fruit Disease

Abstract Objectives The purpose of this work was to evaluate the potential application of papers containing 1-methylcyclopropene (1-MCP) postharvest treatment for suppressing fruit decay of fresh Anxi persimmons and its possible mechanism. Materials and methods Anxi persimmon fruit were treated with papers containing 1-MCP at the dosage of 1.35 μL/L and stored at 25 ± 1 °C and 85 per cent relative humidity for 35 days. During storage, the fruit decay rate and lignin content were evaluated, and the content of total phenolics, the activities of phenylalanine ammonia lyase (PAL), polyphenol oxidase (PPO), peroxidase (POD), chitinase (CHI), and β-1,3-glucanase (GLU) were determined by spectrophotometry. Results The 1-MCP–treated persimmons displayed a lower fruit decay rate, but higher contents of lignin and total phenolics, higher activities of PAL, PPO, POD, CHI, and GLU. Conclusions The treatment with 1-MCP could inhibit the fruit decay of postharvest Anxi persimmons, which might be because 1-MCP enhanced fruit disease resistance by increasing the activities of disease resistance-associated enzymes and retaining higher contents of disease resistance-related substances in postharvest fresh Anxi persimmons. These findings indicate that papers containing 1-MCP at the dosage of 1.35 μL/L have potential application in suppressing fruit decay and extending storage life of postharvest fresh Anxi persimmons.

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dl-β-Aminobutyric Acid–Induced Resistance of Potato Against Phytophthora infestans Requires Salicylic Acid but Not Oxylipins

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-23-5-0585 ◽

2010 ◽

Vol 23 (5) ◽

pp. 585-592 ◽

Cited By ~ 23

Author(s):

Lennart Eschen-Lippold ◽

Simone Altmann ◽

Sabine Rosahl

Keyword(s):

Salicylic Acid ◽

Phytophthora Infestans ◽

Induced Resistance ◽

Crop Plants ◽

Aminobutyric Acid ◽

Systemic Resistance ◽

Lipoxygenase Pathway ◽

Promising Alternative ◽

Functional Analyses ◽

Late Blight Pathogen

Inducing systemic resistance responses in crop plants is a promising alternative way of disease management. To understand the underlying signaling events leading to induced resistance, functional analyses of plants defective in defined signaling pathway steps are required. We used potato, one of the economically most-important crop plants worldwide, to examine systemic resistance against the devastating late blight pathogen Phytophthora infestans, induced by treatment with dl-β-aminobutyric acid (BABA). Transgenic plants impaired in either the 9-lipoxygenase pathway, which produces defense-related compounds, or the 13-lipoxygenase pathway, which generates jasmonic acid–derived signals, expressed wild-type levels of BABA-induced resistance. Plants incapable of accumulating salicylic acid (SA), on the other hand, failed to mount this type of induced resistance. Consistently, treatment of these plants with the SA analog 2,6-dichloroisonicotinic acid restored BABA-induced resistance. Together, these results demonstrate the indispensability of a functional SA pathway for systemic resistance in potato induced by BABA.

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