Resistance to Pseudomonas syringae conferred by an Arabidopsis thaliana coronatine‐insensitive (coi1) mutation occurs through two distinct mechanisms

Kloek, Andrew P.; Verbsky, Michelle L.; Sharma, Sandeep; Schoelz, James E.; Vogel, John P.; Klessig, Daniel F.; Kunkel, Barbara N.

doi:10.1046/j.1365-313x.2001.01050.x

Cited by 310 publications

(322 citation statements)

References 74 publications

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“…In this pathosystem, it is thought that pathogen-secreted COR acts as a mimic of endogenous JA signaling, to suppress SA-dependent defense and promote disease susceptibility. The lack of disease in COR-producing P. syringae-inoculated coi1 plants has been shown to be associated with a faster and stronger induction of PR1, and with an increased accumulation of SA, compared with wild-type plants (Feys et al, 1994;Kloek et al, 2001). In contrast, our experiments revealed that coi1-mediated F. oxysporum resistance was not a result of SA-dependent defense, as coi1/NahG plants were free from lesion development, and were indistinguishable from coi1 plants.…”

Section: Discussioncontrasting

confidence: 51%

“…Although it is not known if coi1 provides resistance to all F. oxysporum strains that are pathogenic on Arabidopsis, our results, and those of others (A. Diener, 13th Congress on Molecular Plant-Microbe Interactions, 2007, Department of Molecular, Cell and Development Biology, University of California, LA, USA), suggest that coi1 resistance is not limited to any particular strain of F. oxysporum. The coi1 mutant also fails to develop chlorotic disease symptoms in response to inoculation with COR-producing P. syringae (Feys et al, 1994;Kloek et al, 2001). In this pathosystem, it is thought that pathogen-secreted COR acts as a mimic of endogenous JA signaling, to suppress SA-dependent defense and promote disease susceptibility.…”

Section: Discussionmentioning

confidence: 99%

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Fusarium oxysporum hijacks COI1‐mediated jasmonate signaling to promote disease development in Arabidopsis

Thatcher

Manners

Kazan³

2009

The Plant Journal

261

295

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SUMMARYAlthough defense responses mediated by the plant oxylipin jasmonic acid (JA) are often necessary for resistance against pathogens with necrotrophic lifestyles, in this report we demonstrate that jasmonate signaling mediated through COI1 in Arabidopsis thaliana is responsible for susceptibility to wilt disease caused by the root-infecting fungal pathogen Fusarium oxysporum. Despite compromised JA-dependent defense responses, the JA perception mutant coronatine insensitive 1 (coi1), but not JA biosynthesis mutants, exhibited a high level of resistance to wilt disease caused by F. oxysporum. This response was independent from salicylic acid-dependent defenses, as coi1/NahG plants showed similar disease resistance to coi1 plants. Inoculation of reciprocal grafts made between coi1 and wild-type plants revealed that coi1-mediated resistance occurred primarily through the coi1 rootstock tissues. Furthermore, microscopy and quantification of fungal DNA during infection indicated that coi1-mediated resistance was not associated with reduced fungal penetration and colonization until a late stage of infection, when leaf necrosis was highly developed in wild-type plants. In contrast to wild-type leaves, coi1 leaves showed no necrosis following the application of F. oxysporum culture filtrate, and showed reduced expression of senescence-associated genes during disease development, suggesting that coi1 resistance is most likely achieved through the inhibition of F. oxysporum-incited lesion development and plant senescence. Together, our results indicate that F. oxysporum hijacks non-defensive aspects of the JA-signaling pathway to cause wilt-disease symptoms that lead to plant death in Arabidopsis.

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Section: Discussioncontrasting

confidence: 51%

Section: Discussionmentioning

confidence: 99%

Fusarium oxysporum hijacks COI1‐mediated jasmonate signaling to promote disease development in Arabidopsis

Thatcher

Manners

Kazan³

2009

The Plant Journal

261

295

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“…The F. oxysporum effector Fo5176-SECRETED IN XYLEM4 also promotes increased disease symptom development through a mechanism yet to be discovered, but it is suggested it may act with other Fo5176 effectors to activate components of the JA-signaling pathway (Thatcher et al, 2012). Other isolates of F. oxysporum and Pseudomonas syringae seem to target host JA signaling by secreting oxylipins or coronatine that mimic the host's endogenous JA signal (Miersch et al, 1999;Kloek et al, 2001;Katsir et al, 2008;Thatcher et al, 2009). These studies detail a common theme where pathogens selectively target host susceptibility genes to cause disease.…”

Section: Discussionmentioning

confidence: 99%

The Lateral Organ Boundaries Domain Transcription Factor LBD20 Functions in Fusarium Wilt Susceptibility and Jasmonate Signaling in Arabidopsis

et al. 2012

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The LATERAL ORGAN BOUNDARIES (LOB) DOMAIN (LBD) gene family encodes plant-specific transcriptional regulators functioning in organ development. In a screen of Arabidopsis (Arabidopsis thaliana) sequence-indexed transferred DNA insertion mutants, we found disruption of the LOB DOMAIN-CONTAINING PROTEIN20 (LBD20) gene led to increased resistance to the root-infecting vascular wilt pathogen Fusarium oxysporum. In wild-type plants, LBD20 transcripts were barely detectable in leaves but abundant in roots, where they were further induced after F. oxysporum inoculation or methyl jasmonate treatment. Induction of LBD20 expression in roots was abolished in coronatine insensitive1 (coi1) and myc2 (allelic to jasmonate insensitive1) mutants, suggesting LBD20 may function in jasmonate (JA) signaling. Consistent with this, expression of the JA-regulated THIONIN2.1 (Thi2.1) and VEGETATIVE STORAGE PROTEIN2 (VSP2) genes were up-regulated in shoots of lbd20 following treatment of roots with F. oxysporum or methyl jasmonate. However, PLANT DEFENSIN1.2 expression was unaltered, indicating a repressor role for LBD20 in a branch of the JA-signaling pathway. Plants overexpressing LBD20 (LBD20-OX) had reduced Thi2.1 and VSP2 expression. There was a significant correlation between increased LBD20 expression in the LBD20-OX lines with both Thi2.1 and VSP2 repression, and reduced survival following F. oxysporum infection. Chlorosis resulting from application of F. oxysporum culture filtrate was also reduced in lbd20 leaves relative to the wild type. Taken together, LBD20 is a F. oxysporum susceptibility gene that appears to regulate components of JA signaling downstream of COI1 and MYC2 that are required for full elicitation of F. oxysporum-and JA-dependent responses. To our knowledge, this is the first demonstration of a role for a LBD gene family member in either biotic stress or JA signaling.

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“…In this case, the absence of gene activation in one mutant could be due to lack of activation functions sensitive to this pathway. Alternatively, because both pathways display mutual antagonistic interactions (Schenk et al, 2000;Kloek et al, 2001;Glazebrook et al, 2003;Spoel et al, 2003), the absence of gene activation could be due to active signaling by the opposite pathway. In this case, repression or lack of induction of genes from Group 3 in infected jar1-1 plants could be due to exacerbation of SA-sensitive responses, whereas down-regulation of genes from Smith et al (2004).…”

Section: Experimental Systemmentioning

confidence: 99%

“…Under several infection conditions, the SA and JA/ET pathways display mutual repression mechanisms (Schenk et al, 2000;Kloek et al, 2001;Glazebrook et al, 2003;Spoel et al, 2003;Bostock, 2005). These pathways regulate host responses in a variety of ways depending on the timing and magnitude of JA/ET and SA accumulation, as well as cross-talk between these pathways and with other yet-unknown regulatory mechanisms (De Vos et al, 2005).…”

Section: Changes Independent From Npr1 and Jar1mentioning

confidence: 99%

Genome-Wide Expression Profiling Arabidopsis at the Stage ofGolovinomyces cichoracearumHaustorium Formation

et al. 2008

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(T.S., K.D.)Compatibility between plants and obligate biotrophic fungi requires fungal mechanisms for efficiently obtaining nutrients and counteracting plant defenses under conditions that are expected to induce changes in the host transcriptome. A key step in the proliferation of biotrophic fungi is haustorium differentiation. Here we analyzed global gene expression patterns in Arabidopsis thaliana leaves during the formation of haustoria by Golovinomyces cichoracearum. At this time, the endogenous levels of salicylic acid (SA) and jasmonic acid (JA) were found to be enhanced. The responses of wild-type, npr1-1, and jar1-1 plants were used to categorize the sensitivity of gene expression changes to NPR1 and JAR1, which are components of the SA and JA signaling pathways, respectively. We found that the infection process was the major source of variation, with 70 genes identified as having similarly altered expression patterns regardless of plant genotype. In addition, principal component analysis (PCA) identified genes responding both to infection and to lack of functional JAR1 (17 genes) or NPR1 (18 genes), indicating that the JA and SA signaling pathways function as secondary sources of variation. Participation of these genes in the SA or JA pathways had not been described previously. We found that some of these genes may be sensitive to the balance between the SA and JA pathways, representing novel markers for the elucidation of cross-talk points between these signaling cascades. Conserved putative regulatory motifs were found in the promoter regions of each subset of genes. Collectively, our results indicate that gene expression changes in response to infection by obligate biotrophic fungi may support fungal nutrition by promoting alterations in host metabolism. In addition, these studies provide novel markers for the characterization of defense pathways and susceptibility features under this infection condition.

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Resistance to Pseudomonas syringae conferred by an Arabidopsis thaliana coronatine‐insensitive (coi1) mutation occurs through two distinct mechanisms

Cited by 310 publications

References 74 publications

Fusarium oxysporum hijacks COI1‐mediated jasmonate signaling to promote disease development in Arabidopsis

Fusarium oxysporum hijacks COI1‐mediated jasmonate signaling to promote disease development in Arabidopsis

The Lateral Organ Boundaries Domain Transcription Factor LBD20 Functions in Fusarium Wilt Susceptibility and Jasmonate Signaling in Arabidopsis

Genome-Wide Expression Profiling Arabidopsis at the Stage ofGolovinomyces cichoracearumHaustorium Formation

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