scholarly journals Systemic Acquired Resistance in Canola Is Linked with Pathogenesis-Related Gene Expression and Requires Salicylic Acid

2007 ◽  
Vol 97 (7) ◽  
pp. 794-802 ◽  
Author(s):  
Shobha D. Potlakayala ◽  
Darwin W. Reed ◽  
Patrick S. Covello ◽  
Pierre R. Fobert
Keyword(s):  
Salicylic Acid ◽  
Pseudomonas Syringae ◽  
Systemic Acquired Resistance ◽  
Induced Defense ◽  
Acquired Resistance ◽  
Microbial Pathogens ◽  
Broad Host Range ◽  
Avirulent Strain ◽  
Enhanced Resistance ◽  
Pathogenesis Related

Systemic acquired resistance (SAR) is an induced defense response that confers long-lasting protection against a broad range of microbial pathogens. Here we show that treatment of Brassica napus plants with the SAR-inducing chemical benzo-(1,2,3)-thiadiazole-7-carbothioic acid S-methyl ester (BTH) significantly enhanced resistance against virulent strains of the bacterial pathogen Pseudomonas syringae pv. maculicola and the fungal pathogen Leptosphaeria maculans. Localized preinoculation of plants with an avirulent strain of P. syringae pv. maculicola also enhanced resistance to these pathogens but was not as effective as BTH treatment. Single applications of either SAR-inducing pretreatment were effective against P. syringae pv. maculicola, even when given more than 3 weeks prior to the secondary challenge. The pretreatments also led to the accumulation of pathogenesis-related (PR) genes, including BnPR-1 and BnPR-2, with higher levels of transcripts observed in the BTH-treatment material. B. napus plants expressing a bacterial salicylate hydroxylase transgene (NahG) that metabolizes salicylic acid to catechol were substantially compromised in SAR and accumulated reduced levels of PR gene transcripts when compared with untransformed controls. Thus, SAR in B. napus displays many of the hallmarks of classical SAR including long lasting and broad host range resistance, association with PR gene activation, and a requirement for salicylic acid.

scholarly journals Induce the plant resistance to pathogen infection

2014 ◽  
Vol 20 (1-2) ◽  
Author(s):  
A. Ezzat ◽  
Z. Szabó ◽  
J. Nyéki
Keyword(s):  
Gene Expression ◽  
Salicylic Acid ◽  
Systemic Acquired Resistance ◽  
Induced Defense ◽  
Acquired Resistance ◽  
Vital Role ◽  
Signal Molecule ◽  
Pathogenesis Related ◽  
Related Proteins ◽  
Direct Toxicity

Systemic acquired resistance (SAR) is a mechanism of induced defense that confers long-lasting protection against a broad spectrum of microorganisms. Salicylic acid (SA) is the signal molecule which is required for induce SAR and is associated with accumulation of pathogenesis-related proteins, which are thought to contribute to resistance. SA paly vital role in some related resistance gene expression in plant cell which have direct or indirect effect on pathogen growth as SA has direct toxicity for pathogen and in the same time has stimulation effect for some enzyme related to reduce the oxidative burst.

scholarly journals Pseudomonas syringae Elicits Emission of the Terpenoid (E,E)-4,8,12-Trimethyl-1,3,7,11-Tridecatetraene in Arabidopsis Leaves Via Jasmonate Signaling and Expression of the Terpene Synthase TPS4

2008 ◽  
Vol 21 (11) ◽  
pp. 1482-1497 ◽  
Author(s):  
Elham Attaran ◽  
Michael Rostás ◽  
Jürgen Zeier
Keyword(s):  
Pseudomonas Syringae ◽  
Systemic Acquired Resistance ◽  
Induced Defense ◽  
Acquired Resistance ◽  
Bacterial Pathogen ◽  
Microbial Pathogens ◽  
Terpene Synthase ◽  
Knockout Mutant ◽  
Direct Role ◽  
Ja Signaling

Volatile, low–molecular weight terpenoids have been implicated in plant defenses, but their direct role in resistance against microbial pathogens is not clearly defined. We have examined a possible role of terpenoid metabolism in the induced defense of Arabidopsis thaliana plants against leaf infection with the bacterial pathogen Pseudomonas syringae. Inoculation of plants with virulent or avirulent P. syringae strains induces the emission of the terpenoids (E,E)-4,8,12-trimethyl-1,3,7,11-tridecatetraene (TMTT), β-ionone and α-farnesene. While the most abundant volatile, the C16-homoterpene TMTT, is produced relatively early in compatible and incompatible interactions, emission of both β-ionone and α-farnesene only increases in later stages of the compatible interaction. Pathogen-induced synthesis of TMTT is controlled through jasmonic acid (JA)-dependent signaling but is independent of a functional salicylic acid (SA) pathway. We have identified Arabidopsis T-DNA insertion lines with defects in the terpene synthase gene TPS4, which is expressed in response to P. syringae inoculation. The tps4 knockout mutant completely lacks induced emission of TMTT but is capable of β-ionone and α-farnesene production, demonstrating that TPS4 is specifically involved in TMTT formation. The tps4 plants display at least wild type–like resistance against P. syringae, indicating that TMTT per se does not protect against the bacterial pathogen in Arabidopsis leaves. Similarly, the ability to mount SA-dependent defenses and systemic acquired resistance (SAR) is barely affected in tps4, which excludes a signaling function of TMTT during SAR. Besides P. syringae challenge, intoxication of Arabidopsis leaves with copper sulfate, a treatment that strongly activates JA biosynthesis, triggers production of TMTT, β-ionone, and α-farnesene. Taken together, our data suggest that induced TMTT production in Arabidopsis is a by-product of activated JA signaling, rather than an effective defense response that contributes to resistance against P. syringae.

scholarly journals Signaling Crosstalk between Salicylic Acid and Ethylene/Jasmonate in Plant Defense: Do We Understand What They Are Whispering?

2019 ◽  
Vol 20 (3) ◽  
pp. 671 ◽  
Author(s):  
Ning Li ◽  
Xiao Han ◽  
Dan Feng ◽  
Deyi Yuan ◽  
Li-Jun Huang
Keyword(s):  
Salicylic Acid ◽  
Signaling Pathways ◽  
Pseudomonas Syringae ◽  
Defense Response ◽  
Systemic Acquired Resistance ◽  
Acquired Resistance ◽  
Defense Responses ◽  
Host Cells ◽  
Defense Gene Expression ◽  
Signaling Crosstalk

During their lifetime, plants encounter numerous biotic and abiotic stresses with diverse modes of attack. Phytohormones, including salicylic acid (SA), ethylene (ET), jasmonate (JA), abscisic acid (ABA), auxin (AUX), brassinosteroid (BR), gibberellic acid (GA), cytokinin (CK) and the recently identified strigolactones (SLs), orchestrate effective defense responses by activating defense gene expression. Genetic analysis of the model plant Arabidopsis thaliana has advanced our understanding of the function of these hormones. The SA- and ET/JA-mediated signaling pathways were thought to be the backbone of plant immune responses against biotic invaders, whereas ABA, auxin, BR, GA, CK and SL were considered to be involved in the plant immune response through modulating the SA-ET/JA signaling pathways. In general, the SA-mediated defense response plays a central role in local and systemic-acquired resistance (SAR) against biotrophic pathogens, such as Pseudomonas syringae, which colonize between the host cells by producing nutrient-absorbing structures while keeping the host alive. The ET/JA-mediated response contributes to the defense against necrotrophic pathogens, such as Botrytis cinerea, which invade and kill hosts to extract their nutrients. Increasing evidence indicates that the SA- and ET/JA-mediated defense response pathways are mutually antagonistic.

scholarly journals rgs-CaM Detects and Counteracts Viral RNA Silencing Suppressors in Plant Immune Priming

2017 ◽  
Vol 91 (19) ◽  
Author(s):  
Eun Jin Jeon ◽  
Kazuki Tadamura ◽  
Taiki Murakami ◽  
Jun-ichi Inaba ◽  
Bo Min Kim ◽  
...  
Keyword(s):  
Salicylic Acid ◽  
Virus Infection ◽  
Virulence Factor ◽  
Rna Silencing ◽  
Systemic Acquired Resistance ◽  
Secondary Infection ◽  
Acquired Resistance ◽  
Tobacco Plants ◽  
Enhanced Resistance ◽  
Salicylic Acid Signaling

ABSTRACT Primary infection of a plant with a pathogen that causes high accumulation of salicylic acid in the plant typically via a hypersensitive response confers enhanced resistance against secondary infection with a broad spectrum of pathogens, including viruses. This phenomenon is called systemic acquired resistance (SAR), which is a plant priming for adaption to repeated biotic stress. However, the molecular mechanisms of SAR-mediated enhanced inhibition, especially of virus infection, remain unclear. Here, we show that SAR against cucumber mosaic virus (CMV) in tobacco plants (Nicotiana tabacum) involves a calmodulin-like protein, rgs-CaM. We previously reported the antiviral function of rgs-CaM, which binds to and directs degradation of viral RNA silencing suppressors (RSSs), including CMV 2b, via autophagy. We found that rgs-CaM-mediated immunity is ineffective against CMV infection in normally growing tobacco plants but is activated as a result of SAR induction via salicylic acid signaling. We then analyzed the effect of overexpression of rgs-CaM on salicylic acid signaling. Overexpressed and ectopically expressed rgs-CaM induced defense reactions, including cell death, generation of reactive oxygen species, and salicylic acid signaling. Further analysis using a combination of the salicylic acid analogue benzo-(1,2,3)-thiadiazole-7-carbothioic acid S-methyl ester (BTH) and the Ca2+ ionophore A23187 revealed that rgs-CaM functions as an immune receptor that induces salicylic acid signaling by simultaneously perceiving both viral RSS and Ca2+ influx as infection cues, implying its autoactivation. Thus, secondary infection of SAR-induced tobacco plants with CMV seems to be effectively inhibited through 2b recognition and degradation by rgs-CaM, leading to reinforcement of antiviral RNA silencing and other salicylic acid-mediated antiviral responses. IMPORTANCE Even without an acquired immune system like that in vertebrates, plants show enhanced whole-plant resistance against secondary infection with pathogens; this so-called systemic acquired resistance (SAR) has been known for more than half a century and continues to be extensively studied. SAR-induced plants strongly and rapidly express a number of antibiotics and pathogenesis-related proteins targeted against secondary infection, which can account for enhanced resistance against bacterial and fungal pathogens but are not thought to control viral infection. This study showed that enhanced resistance against cucumber mosaic virus is caused by a tobacco calmodulin-like protein, rgs-CaM, which detects and counteracts the major viral virulence factor (RNA silencing suppressor) after SAR induction. rgs-CaM-mediated SAR illustrates the growth versus defense trade-off in plants, as it targets the major virulence factor only under specific biotic stress conditions, thus avoiding the cost of constitutive activation while reducing the damage from virus infection.

scholarly journals Isolation of New Arabidopsis Mutants With Enhanced Disease Susceptibility to Pseudomonas syringae by Direct Screening

Genetics ◽  
1998 ◽  
Vol 149 (2) ◽  
pp. 537-548
Author(s):  
Sigrid M Volko ◽  
Thomas Boller ◽  
Frederick M Ausubel
Keyword(s):  
Pseudomonas Syringae ◽  
Fungal Pathogen ◽  
Systemic Acquired Resistance ◽  
Disease Susceptibility ◽  
Acquired Resistance ◽  
Bacterial Pathogen ◽  
Avirulent Strain ◽  
Resistance Response ◽  
Arabidopsis Mutants ◽  
Pathogen Response

Abstract To identify plant defense components that are important in restricting the growth of virulent pathogens, we screened for Arabidopsis mutants in the accession Columbia (carrying the transgene BGL2-GUS) that display enhanced disease susceptibility to the virulent bacterial pathogen Pseudomonas syringae pv. maculicola (Psm) ES4326. Among six (out of a total of 11 isolated) enhanced disease susceptibility (eds) mutants that were studied in detail, we identified one allele of the previously described npr1/nim1/sai1 mutation, which is affected in mounting a systemic acquired resistance response, one allele of the previously identified EDS5 gene, and four EDS genes that have not been previously described. The six eds mutants studied in detail (npr1-4, eds5-2, eds10-1, eds11-1, eds12-1, and eds13-1) displayed different patterns of enhanced susceptibility to a variety of phytopathogenic bacteria and to the obligate biotrophic fungal pathogen Erysiphe orontii, suggesting that particular EDS genes have pathogen-specific roles in conferring resistance. All six eds mutants retained the ability to mount a hypersensitive response and to restrict the growth of the avirulent strain Psm ES4326/avrRpt2. With the exception of npr1-4, the mutants were able to initiate a systemic acquired resistance (SAR) response, although enhanced growth of Psm ES4326 was still detectable in leaves of SAR-induced plants. The data presented here indicate that eds genes define a variety of components involved in limiting pathogen growth, that many additional EDS genes remain to be discovered, and that direct screens for mutants with altered susceptibility to pathogens are helpful in the dissection of complex pathogen response pathways in plants.

scholarly journals Arabidopsis thaliana EDS4 Contributes to Salicylic Acid (SA)-Dependent Expression of Defense Responses: Evidence for Inhibition of Jasmonic Acid Signaling by SA

2000 ◽  
Vol 13 (5) ◽  
pp. 503-511 ◽  
Author(s):  
Vaijayanti Gupta ◽  
Michael G. Willits ◽  
Jane Glazebrook
Keyword(s):  
Gene Expression ◽  
Salicylic Acid ◽  
Jasmonic Acid ◽  
Pseudomonas Syringae ◽  
Systemic Acquired Resistance ◽  
Acquired Resistance ◽  
Defense Responses ◽  
Avirulence Gene ◽  
Signal Molecule ◽  
Resistance Response

The Arabidopsis enhanced disease susceptibility 4 (eds4) mutation causes enhanced susceptibility to infection by the bacterial pathogen Pseudomonas syringae pv. Maculicola ES4326 (Psm ES4326). Gene-for-gene resistance to bacteria carrying the avirulence gene avrRpt2 is not significantly affected by eds4. Plants homozygous for eds4 exhibit reduced expression of the pathogenesis-related gene PR-1 after infection by Psm ES4326, weakened responses to treatment with the signal molecule salicylic acid (SA), impairment of the systemic acquired resistance response, and reduced accumulation of SA after infection with Psm ES4326. These phenotypes indicate that EDS4 plays a role in SA-dependent signaling. SA has been shown to have a negative effect on activation of gene expression by the signal molecule jasmonic acid (JA). Two mutations that cause reduced SA levels, eds4 and pad4, cause heightened responses to inducers of JA-dependent gene expression, providing genetic evidence to support the idea that SA interferes with JA-dependent signaling. Two possible working models of the role of EDS4 in governing activation of defense responses are presented.

Calmodulin-Binding Protein 60b is a central transcriptional activator of immunity

2021 ◽  
Author(s):  
Lu-Shen Li ◽  
Jun Ying ◽  
En Li ◽  
Ting Ma ◽  
Min Li ◽  
...  
Keyword(s):  
Systemic Acquired Resistance ◽  
Binding Protein ◽  
Induced Defense ◽  
Acquired Resistance ◽  
Transcriptional Activator ◽  
Membrane Receptors ◽  
Microbial Pathogens ◽  
Loss Of Function ◽  
Gain Of Function ◽  
Calmodulin Binding

Abstract Plants use a dual defense system to cope with microbial pathogens. The first involves pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) which is conferred by membrane receptors, and the second involves effector-triggered immunity (ETI), which is conferred by disease-resistance proteins (nucleotide-binding leucine-rich repeat containing proteins; NLRs). Calmodulin-Binding Protein 60 (CBP60) family transcription factors are crucial for pathogen defense: CBP60g and Systemic Acquired Resistance Deficient 1 (SARD1) positively regulate immunity, whereas CBP60a negatively regulates immunity. The roles of other Arabidopsis (Arabidopsis thaliana) CBP60s remain unclear. We report that CBP60b positively regulates immunity, and is redundant with—yet distinct from—CBP60g and SARD1. By combining ChIP-PCRs and luciferase (LUC) reporter assays, we demonstrate that CBP60b is a transcriptional activator of immunity genes. Surprisingly, CBP60b loss-of-function results in autoimmunity, exhibiting a phenotype similar to that of CBP60b gain-of-function. Mutations at the EDS1-PAD4-dependent (ENHANCED DISEASE SUSCEPTIBILITY 1– PHYTOALEXIN DEFICIENT 4) ETI pathway fully suppressed the defects of CBP60b loss-of-function but not those of CBP60b gain-of-function, suggesting that CBP60b is monitored by NLRs. Functional loss of SUPPRESSOR OF NPR1-1, CONSTITUTIVE 1 (SNC1), an R-gene, partially rescued the phenotype of cbp60b, further supporting that CBP60b is a protein targeted by pathogen effectors, i.e., a guardee. Unlike CBP60g and SARD1, CBP60b is constitutively and highly expressed in unchallenged plants. Transcriptional and genetic studies further suggest that CBP60b plays a role redundant with CBP60g and SARD1 in pathogen-induced defense, whereas CBP60b has a distinct role in basal defense, partially via direct regulation of CBP60g and SARD1.

scholarly journals Altering Expression of Benzoic Acid/Salicylic Acid Carboxyl Methyltransferase 1 Compromises Systemic Acquired Resistance and PAMP-Triggered Immunity in Arabidopsis

2010 ◽  
Vol 23 (1) ◽  
pp. 82-90 ◽  
Author(s):  
Po-Pu Liu ◽  
Yue Yang ◽  
Eran Pichersky ◽  
Daniel F. Klessig
Keyword(s):  
Salicylic Acid ◽  
Benzoic Acid ◽  
Pseudomonas Syringae ◽  
Systemic Acquired Resistance ◽  
Transgenic Arabidopsis ◽  
Acquired Resistance ◽  
Pathogen Infection ◽  
Carboxyl Methyltransferase ◽  
Effector Triggered Immunity ◽  
Methyltransferase 1

Methyl salicylate (MeSA), which is synthesized in plants from salicylic acid (SA) by methyltransferases, has roles in defense against microbial and insect pests. Most of the MeSA that accumulates after pathogen attack is synthesized by benzoic acid/SA carboxyl methyltransferase 1 (AtBSMT1). To investigate the role of AtBSMT1 in plant defense, transgenic Arabidopsis with altered AtBSMT1 function or expression were assessed for their ability to resist pathogen infection. A knockout mutant (Atbsmt1) failed to accumulate MeSA following pathogen infection; these plants also failed to accumulate SA or its glucoside in the uninoculated leaves and did not develop systemic acquired resistance (SAR). However, the Atbsmt1 mutant exhibited normal levels of effector-triggered immunity and pathogen-associated molecular pattern (PAMP)-triggered immunity to Pseudomonas syringae and Hyaloperonospora arabidopsidis. Analyses of transgenic Arabidopsis plants overexpressing AtBSMT1 revealed that they accumulate elevated levels of MeSA in pathogen-infected leaves but fail to develop SAR. Since the levels of SA and its glucoside were reduced in uninoculated systemic leaves of these plants whereas MeSA levels were elevated, AtBSMT1-mediated conversion of SA to MeSA probably compromised SAR development by suppressing SA accumulation in uninoculated leaves. PAMP-triggered immunity also was compromised in the AtBSMT1 overexpressing plants, although effector-triggered immunity was not.

scholarly journals Research progress of NPR genes in signal pathway of salicylic acid mediated plant disease resistance

2020 ◽  
Vol 145 ◽  
pp. 01038
Author(s):  
Pan Wang ◽  
Meiqin Xiang
Keyword(s):  
Salicylic Acid ◽  
Disease Resistance ◽  
Plant Disease Resistance ◽  
Plant Disease ◽  
Systemic Acquired Resistance ◽  
Acquired Resistance ◽  
Signal Transduction Pathway ◽  
Research Progress ◽  
Signal Molecule ◽  
Pathogenesis Related

Salicylic acid (SA) is considered to be an endogenous signal molecule in plants, and it is related to many resistances in plants. In Arabidopsis, Non-expressor of pathogenesis-related gene1 (NPR1) mediates the expression of pathogenesis-related genes (PRs) and systemic acquired resistance (SAR) induced by SA. NPR1 is a key factor in SA signaling pathway, and the research shows that NPR1, NPR3 and NPR4 play a key role in SA mediated plant disease resistance. In this review, the interaction between NPR and transcription factors is discussed, and we also describe the progress of NPR in SA mediated SAR signal transduction pathway, likewise, we introduce the relationship between NPR1 and its paralogues NPR3/NPR4. This paper analyzes the research prospect of NPR as the intersection of multiple signal paths.

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