Metabolism of salicylic acid in wild-type, ugt74f1 and ugt74f2 glucosyltransferase mutants of Arabidopsis thaliana

2008 ◽  
Vol 132 (4) ◽  
pp. 417-425 ◽  
Author(s):  
John V. Dean ◽  
Sean P. Delaney
Keyword(s):  
Arabidopsis Thaliana ◽  
Salicylic Acid ◽  
Wild Type

scholarly journals Cyst Nematode Parasitism of Arabidopsis thaliana Is Inhibited by Salicylic Acid (SA) and Elicits Uncoupled SA-Independent Pathogenesis-Related Gene Expression in Roots

2008 ◽  
Vol 21 (4) ◽  
pp. 424-432 ◽  
Author(s):  
Martin John Evers Wubben ◽  
Jing Jin ◽  
Thomas Josef Baum
Keyword(s):  
Gene Expression ◽  
Arabidopsis Thaliana ◽  
Salicylic Acid ◽  
Plant Defense ◽  
Cyst Nematode ◽  
Wild Type ◽  
Pathogenesis Related ◽  
Nematode Parasitism ◽  
Sa Signaling ◽  
Increased Susceptibility

Compatible plant–nematode interactions involve the formation of an elaborate feeding site within the host root that requires the evasion of plant defense mechanisms by the parasite. Little is known regarding plant defense signaling pathways that limit nematode parasitism during a compatible interaction. Therefore, we utilized Arabidopsis thaliana mutants perturbed in salicylic acid (SA) biosynthesis or signal transduction to investigate the role of SA in inhibiting parasitism by the beet cyst nematode Heterodera schachtii. We determined that SA-deficient mutants (sid2-1, pad4-1, and NahG) exhibited increased susceptibility to H. schachtii. In contrast, SA-treated wild-type plants showed decreased H. schachtii susceptibility. The npr1-2 and npr1-3 mutants, which are impaired in SA signaling, also showed increased susceptibility to H. schachtii, whereas the npr1-suppressor mutation sni1 showed decreased susceptibility. Constitutive pathogenesis-related (PR) gene-expressing mutants (cpr1 and cpr6) did not show altered susceptibility to H. schachtii; however, constitutive PR gene expression was restricted to cpr1 shoots with wild-type levels of PR-1 transcript present in cpr1 roots. Furthermore, we determined that H. schachtii infection elicits SA-independent PR-2 and PR-5 induction in wild-type roots, while PR-1 transcript and total SA levels remained unaltered. This was in contrast to shoots of infected plants where PR-1 transcript abundance and total SA levels were elevated. We conclude that SA acts via NPR1 to inhibit nematode parasitism which, in turn, is negatively regulated by SNI1. Our results show an inverse correlation between root basal PR-1 expression and plant susceptibility to H. schachtii and suggest that successful cyst nematode parasitism may involve a local suppression of SA signaling in roots.

scholarly journals Knockdown of Quinolinate Phosphoribosyltransferase Results in Decreased Salicylic Acid-Mediated Pathogen Resistance in Arabidopsis thaliana

2021 ◽  
Vol 22 (16) ◽  
pp. 8484
Author(s):  
Shengchun Li ◽  
Haiyan Ding ◽  
Yi Deng ◽  
Jiang Zhang
Keyword(s):  
Arabidopsis Thaliana ◽  
Salicylic Acid ◽  
Pseudomonas Syringae ◽  
De Novo ◽  
Oxidative Stress Marker ◽  
Marker Genes ◽  
Avirulent Strain ◽  
Wild Type ◽  
Nad Biosynthesis ◽  
Quinolinate Phosphoribosyltransferase

Nicotinamide adenine dinucleotide (NAD) is a pivotal coenzyme that has emerged as a central hub linking redox equilibrium and signal transduction in living cells. The homeostasis of NAD is required for plant growth, development, and adaption to environmental stresses. Quinolinate phosphoribosyltransferase (QPRT) is a key enzyme in NAD de novo synthesis pathway. T-DNA-based disruption of QPRT gene is embryo lethal in Arabidopsis thaliana. Therefore, to investigate the function of QPRT in Arabidopsis, we generated transgenic plants with decreased QPRT using the RNA interference approach. While interference of QPRT gene led to an impairment of NAD biosynthesis, the QPRT RNAi plants did not display distinguishable phenotypes under the optimal condition in comparison with wild-type plants. Intriguingly, they exhibited enhanced sensitivity to an avirulent strain of Pseudomonas syringae pv. tomato (Pst-avrRpt2), which was accompanied by a reduction in salicylic acid (SA) accumulation and down-regulation of pathogenesis-related genes expression as compared with the wild type. Moreover, oxidative stress marker genes including GSTU24, OXI1, AOX1 and FER1 were markedly repressed in the QPRT RNAi plants. Taken together, these data emphasized the importance of QPRT in NAD biosynthesis and immunity defense, suggesting that decreased antibacterial immunity through the alteration of NAD status could be attributed to SA- and reactive oxygen species-dependent pathways.

scholarly journals Arabidopsis thaliana FLOWERING LOCUS D Is Required for Systemic Acquired Resistance

2013 ◽  
Vol 26 (9) ◽  
pp. 1079-1088 ◽  
Author(s):  
Vijayata Singh ◽  
Shweta Roy ◽  
Mrunmay Kumar Giri ◽  
Ratnesh Chaturvedi ◽  
Zulkarnain Chowdhury ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Salicylic Acid ◽  
Systemic Acquired Resistance ◽  
Acquired Resistance ◽  
Wild Type ◽  
Long Distance ◽  
Epistasis Analysis ◽  
Flowering Locus ◽  
Systemic Accumulation

Localized infection in plants often induces systemic acquired resistance (SAR), which provides long-term protection against subsequent infections. A signal originating in the SAR-inducing organ is transported to the distal organs, where it stimulates salicylic acid (SA) accumulation and priming, a mechanism that results in more robust activation of defenses in response to subsequent pathogen infection. In recent years, several metabolites that promote long-distance SAR signaling have been identified. However, the mechanism or mechanisms by which plants perceive and respond to the SAR signals are largely obscure. Here, we show that, in Arabidopsis thaliana, the FLOWERING LOCUS D (FLD) is required for responding to the SAR signals leading to the systemic accumulation of SA and enhancement of disease resistance. Although the fld mutant was competent in accumulating the SAR-inducing signal, it was unable to respond to the SAR signal that accumulates in petiole exudates of wild-type leaves inoculated with a SAR-inducing pathogen. Supporting FLD's role in systemic SAR signaling, we observed that dehydroabietinal and azelaic acid, two metabolites that, in wild-type plants, promote SAR-associated systemic accumulation of SA and priming, respectively, were unable to promote SAR in the fld mutant. FLD also participates in flowering, where it functions to repress expression of the flowering repressor FLOWERING LOCUS C (FLC). However, epistasis analysis indicates that FLD's function in SAR is independent of FLC.

scholarly journals PAD4-Dependent Antibiosis Contributes to the ssi2-Conferred Hyper-Resistance to the Green Peach Aphid

2010 ◽  
Vol 23 (5) ◽  
pp. 618-627 ◽  
Author(s):  
Joe Louis ◽  
Queena Leung ◽  
Venkatramana Pegadaraju ◽  
John Reese ◽  
Jyoti Shah
Keyword(s):  
Arabidopsis Thaliana ◽  
Salicylic Acid ◽  
Green Peach Aphid ◽  
Insect Behavior ◽  
Antibiotic Activity ◽  
Broad Host Range ◽  
Wild Type ◽  
Elevated Expression ◽  
Insect Reproduction

Myzus persicae, commonly known as green peach aphid (GPA), is a sap-sucking insect with a broad host range. Arabidopsis thaliana responds to GPA infestation with elevated expression of the PHYTOALEXIN DEFICIENT4 (PAD4) gene. Previously, we had demonstrated that the loss of PAD4 gene function compromises Arabidopsis resistance to GPA. In contrast, a mutation in the Arabidopsis SUPPRESSOR OF SALICYLIC ACID INSENSITIVITY2 (SSI2) gene, which encodes a desaturase involved in lipid metabolism, resulted in hyper-resistance to GPA. We demonstrate here that PAD4 is required for the ssi2-dependent heightened resistance to GPA. Based on electrical monitoring of insect behavior and bioassays in which the insect was given a choice between the wild type and the ssi2 mutant, it is concluded that the ssi2-conferred resistance is not due to deterrence of insect settling or feeding from the phloem of the mutant. Instead, hyper-resistance in the ssi2 mutant results from heightened antibiosis that curtails insect reproduction. Petiole exudates collected from uninfested ssi2 plants contain elevated levels of an activity that interferes with aphid reproduction in synthetic diets. PAD4 was required for the accumulation of this antibiotic activity in petiole exudates, supporting the role of PAD4 in phloem-based resistance. Because PAD4 expression is not elevated in the ssi2 mutant, we suggest that basal PAD4 expression contributes to this antibiosis.

scholarly journals Down Regulation of Virulence Factors of Pseudomonas aeruginosa by Salicylic Acid Attenuates Its Virulence on Arabidopsis thaliana and Caenorhabditis elegans

2005 ◽  
Vol 73 (9) ◽  
pp. 5319-5328 ◽  
Author(s):  
B. Prithiviraj ◽  
H. P. Bais ◽  
T. Weir ◽  
B. Suresh ◽  
E. H. Najarro ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Arabidopsis Thaliana ◽  
Salicylic Acid ◽  
Plant Defense ◽  
Virulence Factors ◽  
Target Genes ◽  
Defense Responses ◽  
Infection Model ◽  
Plant Defense Responses ◽  
Wild Type

ABSTRACT Salicylic acid (SA) is a phenolic metabolite produced by plants and is known to play an important role in several physiological processes, such as the induction of plant defense responses against pathogen attack. Here, using the Arabidopsis thaliana-Pseudomonas aeruginosa pathosystem, we provide evidence that SA acts directly on the pathogen, down regulating fitness and virulence factor production of the bacteria. Pseudomonas aeruginosa PA14 showed reduced attachment and biofilm formation on the roots of the Arabidopsis mutants lox2 and cpr5-2, which produce elevated amounts of SA, as well as on wild-type Arabidopsis plants primed with exogenous SA, a treatment known to enhance endogenous SA concentration. Salicylic acid at a concentration that did not inhibit PA14 growth was sufficient to significantly affect the ability of the bacteria to attach and form biofilm communities on abiotic surfaces. Furthermore, SA down regulated three known virulence factors of PA14: pyocyanin, protease, and elastase. Interestingly, P. aeruginosa produced more pyocyanin when infiltrated into leaves of the Arabidopsis transgenic line NahG, which accumulates less SA than wild-type plants. This finding suggests that endogenous SA plays a role in down regulating the synthesis and secretion of pyocyanin in vivo. To further test if SA directly affects the virulence of P. aeruginosa, we used the Caenorhabiditis elegans-P. aeruginosa infection model. The addition of SA to P. aeruginosa lawns significantly diminished the bacterium's ability to kill the worms, without affecting the accumulation of bacteria inside the nematodes' guts, suggesting that SA negatively affects factors that influence the virulence of P. aeruginosa. We employed microarray technology to identify SA target genes. These analyses showed that SA treatment affected expression of 331 genes. It selectively repressed transcription of exoproteins and other virulence factors, while it had no effect on expression of housekeeping genes. Our results indicate that in addition to its role as a signal molecule in plant defense responses, SA works as an anti-infective compound by affecting the physiology of P. aeruginosa and ultimately attenuating its virulence.

Characterization of a Salicylic Acid-Insensitive Mutant (sai1) of Arabidopsis thaliana, Identified in a Selective Screen Utilizing the SA-Inducible Expression of the tms2 Gene

1997 ◽  
Vol 10 (1) ◽  
pp. 69-78 ◽  
Author(s):  
Jyoti Shah ◽  
Frank Tsui ◽  
Daniel F. Klessig
Keyword(s):  
Signal Transduction ◽  
Arabidopsis Thaliana ◽  
Salicylic Acid ◽  
Root Growth ◽  
Signal Transduction Pathway ◽  
Inducible Expression ◽  
Transduction Pathway ◽  
Wild Type ◽  
Pathogen Invasion ◽  
Tms2 Gene

Salicylic acid (SA) plays an important signaling role in the resistance of many plants to pathogen invasion. Increases in endogenous SA levels have been associated with the hypersensitive response as well as systemic acquired resistance (SAR). SA also induces the expression of a subset of the pathogenesis-related (PR) genes. However, relatively little is known about the events occurring subsequent to SA accumulation during a resistance response. In order to identify mutations in components of the SA signal transduction pathway, we have developed a genetic screen in Arabidopsis thaliana that utilizes the Agrobacterium tumefaciens tms2 gene as a counter-selectable marker. SA-inducible expression of the tms2 gene from the tobacco PR-1a promoter confers sensitivity to α-naphthalene acetamide (α-NAM), resulting in inhibition of root growth in germinating transgenic Arabidopsis seedlings. Mutants in which root growth is insensitive to α-NAM have been selected from this PR-1a:tms2 transgenic line with the expectation that a subset will lack a regulatory component downstream of SA. The sai1 mutant so identified expressed neither the PR-1a:tms2 transgene nor the endogenous Arabidopsis PR-1, PR-2, and PR-5 genes in response to SA. These genes also were not induced in sai1 by 2,6-dichloroisonicotinic acid (INA) or benzothiadiazole (BTH), two chemical inducers of SAR. As expected of a mutation acting downstream of SA, sai1 plants accumulate SA and its glucoside in response to infection with an avirulent pathogen and are more susceptible to this avirulent pathogen than the wild-type parent. sai1 is allelic to npr1, a previously identified SA-noninducible mutation. The recessive nature of the noninducible sai1 mutation suggests that the wild-type SAI1 gene acts as a positive regulator in the SA signal transduction pathway.

scholarly journals CRISPR-finder: A high throughput and cost-effective method to identify successfully edited Arabidopsis thaliana individuals

2021 ◽  
Vol 2 ◽  
Author(s):  
Efthymia Symeonidi ◽  
Julian Regalado ◽  
Rebecca Schwab ◽  
Detlef Weigel
Keyword(s):  
Arabidopsis Thaliana ◽  
Salicylic Acid ◽  
High Throughput ◽  
Cost Effective ◽  
Repair Process ◽  
Wild Type ◽  
Isochorismate Synthase ◽  
Guide Rna ◽  
Cost Effective Method ◽  
Variable Efficiency

Abstract Genome editing with the CRISPR/Cas (clustered regularly interspaced short palindromic repeats/CRISPR associated protein) system allows mutagenesis of a targeted region of the genome using a Cas endonuclease and an artificial guide RNA. Both because of variable efficiency with which such mutations arise and because the repair process produces a spectrum of mutations, one needs to ascertain the genome sequence at the targeted locus for many individuals that have been subjected to mutagenesis. We provide a complete protocol for the generation of amplicons up until the identification of the exact mutations in the targeted region. CRISPR-finder can be used to process thousands of individuals in a single sequencing run. We successfully identified an ISOCHORISMATE SYNTHASE 1 mutant line in which the production of salicylic acid was impaired compared to the wild type, as expected. These features establish CRISPR-finder as a high-throughput, cost-effective and efficient genotyping method of individuals whose genomes have been targeted using the CRISPR/Cas9 system.

scholarly journals Salicylic Acid Accumulation Controlled by LSD1 Is Essential in Triggering Cell Death in Response to Abiotic Stress

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 962
Author(s):  
Maciej Jerzy Bernacki ◽  
Anna Rusaczonek ◽  
Weronika Czarnocka ◽  
Stanisław Karpiński
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Abiotic Stress ◽  
Wild Type ◽  
Pr Genes ◽  
Genes Expression ◽  
Salicylic Acid Accumulation ◽  
Cell Death Phenotype ◽  
Insight Into

Salicylic acid (SA) is well known hormonal molecule involved in cell death regulation. In response to a broad range of environmental factors (e.g., high light, UV, pathogens attack), plants accumulate SA, which participates in cell death induction and spread in some foliar cells. LESION SIMULATING DISEASE 1 (LSD1) is one of the best-known cell death regulators in Arabidopsis thaliana. The lsd1 mutant, lacking functional LSD1 protein, accumulates SA and is conditionally susceptible to many biotic and abiotic stresses. In order to get more insight into the role of LSD1-dependent regulation of SA accumulation during cell death, we crossed the lsd1 with the sid2 mutant, caring mutation in ISOCHORISMATE SYNTHASE 1(ICS1) gene and having deregulated SA synthesis, and with plants expressing the bacterial nahG gene and thus decomposing SA to catechol. In response to UV A+B irradiation, the lsd1 mutant exhibited clear cell death phenotype, which was reversed in lsd1/sid2 and lsd1/NahG plants. The expression of PR-genes and the H2O2 content in UV-treated lsd1 were significantly higher when compared with the wild type. In contrast, lsd1/sid2 and lsd1/NahG plants demonstrated comparability with the wild-type level of PR-genes expression and H2O2. Our results demonstrate that SA accumulation is crucial for triggering cell death in lsd1, while the reduction of excessive SA accumulation may lead to a greater tolerance toward abiotic stress.

scholarly journals Inhibition of cell expansion enhances cortical microtubule stability in the root apex of Arabidopsis thaliana

2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Veronica Giourieva ◽  
Emmanuel Panteris
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Wall ◽  
Cell Expansion ◽  
Cortical Microtubule ◽  
Root Apex ◽  
Cellulose Synthase ◽  
Cellulose Biosynthesis ◽  
Cortical Microtubules ◽  
Wild Type ◽  
Microtubule Stability

Abstract Background Cortical microtubules regulate cell expansion by determining cellulose microfibril orientation in the root apex of Arabidopsis thaliana. While the regulation of cell wall properties by cortical microtubules is well studied, the data on the influence of cell wall to cortical microtubule organization and stability remain scarce. Studies on cellulose biosynthesis mutants revealed that cortical microtubules depend on Cellulose Synthase A (CESA) function and/or cell expansion. Furthermore, it has been reported that cortical microtubules in cellulose-deficient mutants are hypersensitive to oryzalin. In this work, the persistence of cortical microtubules against anti-microtubule treatment was thoroughly studied in the roots of several cesa mutants, namely thanatos, mre1, any1, prc1-1 and rsw1, and the Cellulose Synthase Interacting 1 protein (csi1) mutant pom2-4. In addition, various treatments with drugs affecting cell expansion were performed on wild-type roots. Whole mount tubulin immunolabeling was applied in the above roots and observations were performed by confocal microscopy. Results Cortical microtubules in all mutants showed statistically significant increased persistence against anti-microtubule drugs, compared to those of the wild-type. Furthermore, to examine if the enhanced stability of cortical microtubules was due to reduced cellulose biosynthesis or to suppression of cell expansion, treatments of wild-type roots with 2,6-dichlorobenzonitrile (DCB) and Congo red were performed. After these treatments, cortical microtubules appeared more resistant to oryzalin, than in the control. Conclusions According to these findings, it may be concluded that inhibition of cell expansion, irrespective of the cause, results in increased microtubule stability in A. thaliana root. In addition, cell expansion does not only rely on cortical microtubule orientation but also plays a regulatory role in microtubule dynamics, as well. Various hypotheses may explain the increased cortical microtubule stability under decreased cell expansion such as the role of cell wall sensors and the presence of less dynamic cortical microtubules.

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