Local and Systemic Immunity in Plants
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The Arabidopsis Flavin-Dependent Monooxygenase FMO1 Is an Essential Component of Biologically Induced Systemic Acquired Resistance (2006)

The Arabidopsis Flavin-Dependent Monooxygenase FMO1 Is an Essential Component of Biologically Induced Systemic Acquired Resistance (2006) | Local and Systemic Immunity in Plants | Scoop.it

Upon localized attack by necrotizing pathogens, plants gradually develop increased resistance against subsequent infections at the whole-plant level, a phenomenon known as systemic acquired resistance (SAR). To identify genes involved in the establishment of SAR, we pursued a strategy that combined gene expression information from microarray data with pathological characterization of selected Arabidopsis (Arabidopsis thaliana) T-DNA insertion lines. A gene that is up-regulated in Arabidopsis leaves inoculated with avirulent or virulent strains of the bacterial pathogen Pseudomonas syringae  pv  maculicola (Psm) showed homology to flavin-dependent monooxygenases (FMO) and was designated asFMO1. An Arabidopsis knockout line of FMO1 proved to be fully impaired in the establishment of SAR triggered by avirulent (Psm avrRpm1) or virulent (Psm) bacteria. Loss of SAR in the fmo1 mutants was accompanied by the inability to initiate systemic accumulation of salicylic acid (SA) and systemic expression of diverse defense-related genes. In contrast, responses at the site of pathogen attack, including increases in the levels of the defense signals SA and jasmonic acid, camalexin accumulation, and expression of various defense genes, were induced in a similar manner in both fmo1 mutant and wild-type plants. Consistently, the fmo1 mutation did not significantly affect local disease resistance toward virulent or avirulent bacteria in naive plants. Induction of FMO1 expression at the site of pathogen inoculation is independent of SA signaling, but attenuated in the Arabidopsis eds1 and pad4 defense mutants. Importantly, FMO1 expression is also systemically induced upon localized P. syringae infection. This systemic up-regulation is missing in the SAR-defective SA pathway mutants sid2 and npr1, as well as in the defense mutant ndr1, indicating a close correlation between systemic FMO1 expression and SAR establishment. Our findings suggest that the presence of the FMO1 gene product in systemic tissue is critical for the development of SAR, possibly by synthesis of a metabolite required for the transduction or amplification of a signal during the early phases of SAR establishment in systemic leaves.

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The Extent to Which Methyl Salicylate Is Required for Signaling Systemic Acquired Resistance Is Dependent on Exposure to Light after Infection (2011)

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Arabidopsis systemic immunity uses conserved defense signaling pathways and is mediated by jasmonates (2007)

Arabidopsis systemic immunity uses conserved defense signaling pathways and is mediated by jasmonates (2007) | Local and Systemic Immunity in Plants | Scoop.it
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Methyl Salicylate Is a Critical Mobile Signal for Plant Systemic Acquired Resistance (2007)

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An extracellular aspartic protease functions in Arabidopsis disease resistance signaling (2004)

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Accumulation of salicylic acid and PR-1 gene transcripts in relation to the systemic acquired resistance (SAR) response induced by Pseudomonas syringae pv. tomato in Arabidopsis (1999)

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ABSTRACT

The relationship between salicylic acid (SA) accumulation, PR-1 gene expression, and the degree of systemic acquired resistance (SAR) established in Arabidopsis plants has been determined by comparing the response of wild-type ecotype Columbia (Col-0) and two hypersensitive response (HR)-defective mutants (rps2-201 andrps2-101C ) during the SAR response induced by avirulent Pseudomonas syringae pv. tomato(Pst). Unlike wild-type Col-0 plants, plants harboring either mutant allele were unable to manifest a SAR response. During the initiation/immunization stage of SAR, PR-1 gene expression was delayed in interactions which did not lead to SAR (avirulent inoculation of rps2-201 and rps2-101C, or inoculation with virulent bacteria in wild-type Col-0) compared to those interactions that did lead to SAR (avirulent inoculation of wild-type Col-0). PR-1 expression was reduced in the rps mutants compared to wild-type plants during the establishment and manifestation stage and therefore correlated with the ability to elicit a SAR response. SA accumulated to similar levels during the establishment and manifestation stages for Col-0 and therps2mutant alleles. Therefore the ability to accumulate SA was not predictive of the ability to elicit SAR, and SA accumulation alone is not sufficient to elicit the SAR response. Moreover, SA accumulated to similar levels during both compatible (virulent infections) and incompatible interactions (avirulent infections). However, SA accumulation was reduced in the initiation/immunization stage of SAR in rps2-101C compared to wild-type, but not in rps2-201 , suggesting that this reduction was related to an HR-specific defect mediated by the rps2-101C mutant allele.

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A key role for ALD1 in activation of local and systemic defenses in Arabidopsis - Song - 2004

A key role for ALD1 in activation of local and systemic defenses in Arabidopsis - Song - 2004 | Local and Systemic Immunity in Plants | Scoop.it

The Arabidopsis thaliana agd2-like defense response protein1 (ald1) mutant was previously found to be hypersusceptible to the virulent bacterial pathogen Pseudomonas syringae and had reduced accumulation of the defense signal salicylic acid (SA). ALD1 was shown to possess aminotransferase activity in vitro, suggesting it generates an amino acid-derived defense signal. We now find ALD1 to be a key defense component that acts in multiple contexts and partially requires the PHYTOALEXIN DEFICIENT4 (PAD4) defense regulatory gene for its expression in response to infection. ald1 plants have increased susceptibility to avirulent P. syringae strains, are unable to activate systemic acquired resistance and are compromised for resistance to the oomycete pathogen Peronospora parasitica in mutants with constitutively active defenses. ALD1 and PAD4 can act additively to control SA, PATHOGENESIS RELATED GENE1 (PR1) transcript and camalexin (an antimicrobial metabolite) accumulation as well as disease resistance. Finally, ALD1 and PAD4 can mutually affect each other's expression in a constitutive defense mutant, suggesting that these two genes can act in a signal amplification loop.

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Methyl Salicylate Production and Jasmonate Signaling Are Not Essential for Systemic Acquired Resistance in Arabidopsis (2009)

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Identification of likely orthologs of tobacco salicylic acid-binding protein 2 and their role in systemic acquired resistance in Arabidopsis thaliana - Vlot - 2008

Identification of likely orthologs of tobacco salicylic acid-binding protein 2 and their role in systemic acquired resistance in Arabidopsis thaliana - Vlot - 2008 | Local and Systemic Immunity in Plants | Scoop.it
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Characterization of Recombinant CDR1, an Arabidopsis Aspartic Proteinase Involved in Disease Resistance (2007)

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A putative lipid transfer protein involved in systemic resistance signalling in Arabidopsis (2002)

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Salicylic Acid Is Not the Translocated Signal Responsible for Inducing Systemic Acquired Resistance but Is Required in Signal Transduction. (1994)

Salicylic Acid Is Not the Translocated Signal Responsible for Inducing Systemic Acquired Resistance but Is Required in Signal Transduction. (1994) | Local and Systemic Immunity in Plants | Scoop.it
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Seminal SAR Research

 

ABSTRACT: Infection of plants by necrotizing pathogens can induce broad-spectrum resistance to subsequent pathogen infection. This systemic acquired resistance (SAR) is thought to be triggered by a vascular-mobile signal that moves throughout the plant from the infected leaves. A considerable amount of evidence suggests that salicylic acid (SA) is involved in the induction of SAR. Because SA is found in phloem exudate of infected cucumber and tobacco plants, it has been proposed as a candidate for the translocated signal. To determine if SA is the mobile signal, grafting experiments were performed using transgenic plants that express a bacterial SA-degrading enzyme. We show that transgenic tobacco root-stocks, although unable to accumulate SA, were fully capable of delivering a signal that renders nontransgenic scions resistant to further pathogen infection. This result indicated that the translocating, SAR-inducing signal is not SA. Reciprocal grafts demonstrated that the signal requires the presence of SA in tissues distant from the infection site to induce systemic resistance

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