Pseudomonas syringae Type III Effector HopZ1 Targets a Host Enzyme to Suppress Isoflavone Biosynthesis and Promote Infection in Soybean

Zhou, Huanbin; Lin, Jian; Johnson, Aimee; Morgan, Robyn L.; Zhong, Wenwan; Ma, Wenbo

doi:10.1016/j.chom.2011.02.007

Cited by 94 publications

(79 citation statements)

References 55 publications

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“…In a compatible E. amylovora-apple pathosystem, the induced expression of phenylpropanoid pathway genes is delayed in a T3SS-dependent manner (Venisse et al, 2002). P. syringae type III effectors can alter the accumulation of chorismate-and Phe-derived metabolites (Jelenska et al, 2007;Zhou et al, 2011). U. maydis deploys effectors that suppress SA production (Djamei et al, 2011) and promote anthocyanin production (Tanaka et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

“…Some T3Es have been shown to inhibit specific metabolic processes and thus alter the accumulation of specific plant hormones or metabolites. For example, Jelenska et al (2007) showed that a P. syringae T3E, HopI1, inhibits SA production by targeting of a chloroplast-localized chaperone, and Zhou et al (2011) showed that another P. syringae T3E, HopZ1b, suppresses the production of a phytoalexin precursor by targeting a soybean (Glycine max) 2-hydroxyisoflavanone dehydratase. We show here that WtsE alters the expression of an entire suite of metabolic enzymes, which results in the accumulation of CouTyr.…”

Section: Discussionmentioning

confidence: 99%

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Perturbation of Maize Phenylpropanoid Metabolism by an AvrE Family Type III Effector from Pantoea stewartii

et al. 2015

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Republic of Korea (S.-M.P., M.G.K.)AvrE family type III effector proteins share the ability to suppress host defenses, induce disease-associated cell death, and promote bacterial growth. However, despite widespread contributions to numerous bacterial diseases in agriculturally important plants, the mode of action of these effectors remains largely unknown. WtsE is an AvrE family member required for the ability of Pantoea stewartii ssp. stewartii (Pnss) to proliferate efficiently and cause wilt and leaf blight symptoms in maize (Zea mays) plants. Notably, when WtsE is delivered by a heterologous system into the leaf cells of susceptible maize seedlings, it alone produces water-soaked disease symptoms reminiscent of those produced by Pnss. Thus, WtsE is a pathogenicity and virulence factor in maize, and an Escherichia coli heterologous delivery system can be used to study the activity of WtsE in isolation from other factors produced by Pnss. Transcriptional profiling of maize revealed the effects of WtsE, including induction of genes involved in secondary metabolism and suppression of genes involved in photosynthesis. Targeted metabolite quantification revealed that WtsE perturbs maize metabolism, including the induction of coumaroyl tyramine. The ability of mutant WtsE derivatives to elicit transcriptional and metabolic changes in susceptible maize seedlings correlated with their ability to promote disease. Furthermore, chemical inhibitors that block metabolic flux into the phenylpropanoid pathways targeted by WtsE also disrupted the pathogenicity and virulence activity of WtsE. While numerous metabolites produced downstream of the shikimate pathway are known to promote plant defense, our results indicate that misregulated induction of phenylpropanoid metabolism also can be used to promote pathogen virulence.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Perturbation of Maize Phenylpropanoid Metabolism by an AvrE Family Type III Effector from Pantoea stewartii

et al. 2015

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“…T3Es commonly contain sequences addressing specific eukaryotic subcellular localizations (10,11) and enzymatic activities (12)(13)(14)(15)(16)(17) that disrupt and/or suppress PTI. Known targets of T3Es include plasma membrane-localized receptor complexes (13,(18)(19)(20)(21)(22)(23), downstream MAPK cascades (24,25), the stability of defenserelated transcripts (26), phytoalexin biosynthesis (27), and vesicle trafficking (28).…”

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confidence: 99%

Pseudomonas syringae type III effector HopAF1 suppresses plant immunity by targeting methionine recycling to block ethylene induction

Washington

Mukhtar

Finkel

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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HopAF1 is a type III effector protein of unknown function encoded in the genomes of several strains of Pseudomonas syringae and other plant pathogens. Structural modeling predicted that HopAF1 is closely related to deamidase proteins. Deamidation is the irreversible substitution of an amide group with a carboxylate group. Several bacterial virulence factors are deamidases that manipulate the activity of specific host protein substrates. We identified Arabidopsis methylthioadenosine nucleosidase proteins MTN1 and MTN2 as putative targets of HopAF1 deamidation. MTNs are enzymes in the Yang cycle, which is essential for the high levels of ethylene biosynthesis in Arabidopsis. We hypothesized that HopAF1 inhibits the host defense response by manipulating MTN activity and consequently ethylene levels. We determined that bacterially delivered HopAF1 inhibits ethylene biosynthesis induced by pathogenassociated molecular patterns and that Arabidopsis mtn1 mtn2 mutant plants phenocopy the effect of HopAF1. Furthermore, we identified two conserved asparagines in MTN1 and MTN2 from Arabidopsis that confer loss of function phenotypes when deamidated via site-specific mutation. These residues are potential targets of HopAF1 deamidation. HopAF1-mediated manipulation of Yang cycle MTN proteins is likely an evolutionarily conserved mechanism whereby HopAF1 orthologs from multiple plant pathogens contribute to disease in a large variety of plant hosts.

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“…The same result was obtained when isoflavone synthase or chalcone reductase were silenced in soybean (Subramanian et al 2005;Graham et al 2007). Silencing of another enzyme required for isoflavone synthesis resulted in increased susceptibility of soybean to the bacterial pathogen Pseudomonas syringae, (Zhou et al 2011). P. syringae, unlike fungal pathogens, was not inhibited by isoflavones in vitro, suggesting that isoflavones could also have a role in defense signaling (Rivera-Vargas et al 1993;Zhou et al 2011).…”

Section: Flavonoidsmentioning

confidence: 93%

New Antimicrobial Agents of Plant Origin

Sampedro

Valdivia

2013

Antimicrobial Compounds

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Plants are constantly under attack by microbial pathogens. As part of their defensive arsenal, they use antimicrobial peptides such as thionins, defensins, lipid transfer proteins, hevein-like peptides, knottins, cyclotides, b-barrelins, and others. In addition, they produce a diversity of antimicrobial metabolites. Those where the evidence for a role in plant defense is stronger include benzoxazinoids, camalexin, and glucosinolates among the alkaloids; flavonoids and stilbenes among the phenylpropanoids; and also terpenoids such as saponins. Our understanding of these plant antimicrobial agents has increased significantly in recent years with new information on their distribution, synthesis, regulation, in vivo function, and mechanism of action. Plant antimicrobial agents have a large potential for biotechnological applications. Engineered plants with increased disease resistance have been achieved using almost every family of antimicrobial peptides. There have been also been successes in using metabolic engineering to increase the production of antimicrobial compounds, as in the case of stilbenes and glucosinolates. Commercial applications using both approaches are likely to appear soon. The use of plant antimicrobials in human medicine is probably further in the future, although there are promising antifungal agents like defensin peptides, and saponins. With more than a quarter million species and a particularly diverse specialized metabolism, the richness of plant antimicrobials has barely been explored. Plant Antimicrobial DefensesWild plants are quite successful at keeping bacterial and fungal pathogens at bay. In addition to physical barriers, they have an immune system capable of detecting and responding to the presence of pathogens. The first layer of defense is based on

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Pseudomonas syringae Type III Effector HopZ1 Targets a Host Enzyme to Suppress Isoflavone Biosynthesis and Promote Infection in Soybean

Cited by 94 publications

References 55 publications

Perturbation of Maize Phenylpropanoid Metabolism by an AvrE Family Type III Effector from Pantoea stewartii

Perturbation of Maize Phenylpropanoid Metabolism by an AvrE Family Type III Effector from Pantoea stewartii

Pseudomonas syringae type III effector HopAF1 suppresses plant immunity by targeting methionine recycling to block ethylene induction

New Antimicrobial Agents of Plant Origin

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