scholarly journals Arabidopsismlo3mutant plants exhibit spontaneous callose deposition and signs of early leaf senescence

2019 ◽  
Author(s):  
Stefan Kusch ◽  
Susanne Thiery ◽  
Anja Reinstädler ◽  
Katrin Gruner ◽  
Krzysztof Zienkiewicz ◽  
...  
Keyword(s):  
Salicylic Acid ◽  
Powdery Mildew ◽  
Pseudomonas Syringae ◽  
Systemic Acquired Resistance ◽  
Acquired Resistance ◽  
Bacterial Pathogen ◽  
Resistance Locus ◽  
Callose Deposition ◽  
Powdery Mildew Fungi ◽  
Hyaloperonospora Arabidopsidis

The family of Mildew resistance Locus O (MLO) proteins is best known for its profound effect on the outcome of powdery mildew infections: when the appropriate MLO protein is absent, the plant is fully resistant to otherwise virulent powdery mildew fungi. However, most members of the MLO protein family remain functionally unexplored. Here, we investigateArabidopsis thaliana MLO3, the closest relative ofAtMLO2, AtMLO6andAtMLO12, which are the ArabidopsisMLOgenes implicated in the powdery mildew interaction. The co-expression network ofAtMLO3suggests association of the gene with plant defense-related processes such as salicylic acid homeostasis. Our extensive analysis shows thatmlo3mutants are unaffected regarding their infection phenotype upon challenge with the powdery mildew fungiGolovinomyces orontiiandErysiphe pisi, the oomyceteHyaloperonospora arabidopsidis, and the bacterial pathogenPseudomonas syringae(the latter both in terms of basal and systemic acquired resistance), indicating that the protein does not play a major role in the response to any of these pathogens. However,mlo3genotypes display spontaneous callose deposition as well as signs of early senescence in six-or seven-week-old rosette leaves in the absence of any pathogen challenge, a phenotype that is reminiscent ofmlo2mutant plants. We hypothesize that de-regulated callose deposition inmlo3genotypes is the result of a subtle transient aberration of salicylic acid-jasmonic acid homeostasis during development.

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 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 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 UGT76B1 glycosylates N-hydroxy-pipecolic acid and inactivates systemic acquired resistance in tomato

2020 ◽  
Author(s):  
Eric C. Holmes ◽  
Yun-Chu Chen ◽  
Mary Beth Mudgett ◽  
Elizabeth S. Sattely
Keyword(s):  
Pseudomonas Syringae ◽  
Systemic Acquired Resistance ◽  
Acquired Resistance ◽  
Bacterial Pathogen ◽  
Defense Responses ◽  
Pipecolic Acid ◽  
Systemic Resistance ◽  
Biosynthetic Genes ◽  
Solanaceous Plants

AbstractSystemic acquired resistance (SAR) is a mechanism that plants utilize to connect a local pathogen infection to global defense responses. N-hydroxy-pipecolic acid (NHP) and a glycosylated derivative are produced during SAR, yet their individual roles in the response have not yet been elucidated. Here we report that Arabidopsis thaliana UGT76B1 can generate glycosylated NHP (NHP-Glc) in vitro and when transiently expressed alongside Arabidopsis NHP biosynthetic genes in two Solanaceous plants. During infection, Arabidopsis ugt76b1 mutants do not accumulate NHP-Glc and accumulate less glycosylated salicylic acid (SA-Glc) than wild type plants. The metabolic changes in ugt76b1 mutant plants are accompanied by enhanced defense to the bacterial pathogen Pseudomonas syringae, suggesting that glycosylation of SAR molecules NHP and SA by UGT76B1 plays an important role in defense modulation. Transient expression of Arabidopsis UGT76B1 with the Arabidopsis NHP biosynthesis genes ALD1 and FMO1 in tomato increases NHP-Glc production and reduces NHP accumulation in local tissue, and abolishes the systemic resistance seen when expressing NHP-biosynthetic genes alone. These findings reveal that the glycosylation of NHP by UGT76B1 alters defense priming in systemic tissue and provide further evidence for the role of the NHP aglycone as the active metabolite in SAR signaling.

scholarly journals Arabidopsis Clade I TGA Transcription Factors Regulate Plant Defenses in an NPR1-Independent Fashion

2012 ◽  
Vol 25 (11) ◽  
pp. 1459-1468 ◽  
Author(s):  
Heather L. Shearer ◽  
Yu Ti Cheng ◽  
Lipu Wang ◽  
Jinman Liu ◽  
Patrick Boyle ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Pseudomonas Syringae ◽  
Systemic Acquired Resistance ◽  
Acquired Resistance ◽  
Defense Responses ◽  
R Gene ◽  
Triple Mutant ◽  
Transcriptional Reprogramming ◽  
Tga Factors ◽  
Hyaloperonospora Arabidopsidis

Transcriptional reprogramming during induction of salicylic acid (SA)-mediated defenses is regulated primarily by NPR1 (NONEXPRESSOR OF PATHOGENESIS-RELATED GENES 1), likely through interactions with TGA bZIP transcription factors. To ascertain the contributions of clade I TGA factors (TGA1 and TGA4) to defense responses, a tga1-1 tga4-1 double mutant was constructed and challenged with Pseudomonas syringae and Hyaloperonospora arabidopsidis. Although the mutant displayed enhanced susceptibility to virulent P. syringae, it was not compromised in systemic acquired resistance against this pathogen or resistance against avirulent H. arabidopsidis. Microarray analysis of nonelicited and SA-treated plants indicated that clade I TGA factors regulate fewer genes than NPR1. Approximately half of TGA-dependent genes were regulated by NPR1 but, in all cases, the direction of change was opposite in the two mutants. In support of the microarray data, the NPR1-independent disease resistance observed in the autoimmune resistance (R) gene mutant snc1 is partly compromised by tga1-1 tga4-1 mutations, and a triple mutant of clade I TGA factors with npr1-1 is more susceptible than either parent. These results suggest that clade I TGA factors are required for resistance against virulent pathogens and avirulent pathogens mediated by at least some R gene specificities, acting substantially through NPR1-independent pathways.

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.

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 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.

Role of Salicylic Acid and NIM1/NPR1 in Race-Specific Resistance in Arabidopsis

Genetics ◽  
2002 ◽  
Vol 161 (2) ◽  
pp. 803-811
Author(s):  
Gregory J Rairdan ◽  
Terrence P Delaney
Keyword(s):  
Salicylic Acid ◽  
Pseudomonas Syringae ◽  
Leucine Zipper ◽  
Systemic Acquired Resistance ◽  
Specific Resistance ◽  
Strong Dependence ◽  
Acquired Resistance ◽  
R Genes ◽  
Resistance Response

Abstract Salicylic acid (SA) and the NIM1/NPR1 protein have both been demonstrated to be required for systemic acquired resistance (SAR) and implicated in expression of race-specific resistance. In this work, we analyzed the role that each of these molecules play in the resistance response triggered by members of two subclasses of resistance (R) genes, members of which recognize unrelated pathogens. We tested the ability of TIR and coiled-coil-class (also known as leucine-zipper-class) R genes to confer resistance to Pseudomonas syringae pv. tomato or Peronospora parasitica in SA-depleted (NahG) and nim1/npr1 plants. We found that all of the P. syringae pv. tomato-specific R genes tested were dependent upon SA accumulation, while none showed strong dependence upon NIM1/NPR1 activity. A similar SA dependence was observed for the P. parasitica TIR and CC-class R genes RPP5 and RPP8, respectively. However, the P. parasitica-specific R genes differed in their requirement for NIM1/NPR1, with just RPP5 depending upon NIM1/NPR1 activity for effectiveness. These data are consistent with the hypothesis that at least in Arabidopsis, SA accumulation is necessary for the majority of R-gene-triggered resistance, while the role of NIM1/NPR in race-specific resistance is limited to resistance to P. parasitica mediated by TIR-class R genes.

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