Identification and Characterization of a Well-Defined Series of Coronatine Biosynthetic Mutants of <i>Pseudomonas syringae</i> pv. <i>tomato</i> DC3000

Brooks, David; Hernández-Guzmán, Gustavo; Kloek, Andrew P.; Alarcón-Chaidez, Francisco J.; Sreedharan, Aswathy; Rangaswamy, Vidhya; Peñaloza‐Vázquez, Alejandro; Bender, Carol L.; Kunkel, Barbara N.

doi:10.1094/mpmi.2004.17.2.162

Cited by 213 publications

(234 citation statements)

References 59 publications

(103 reference statements)

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“…Infection of Col-0 leaves with the coronatine-producing Pst wild-type strain evoked a strong emission of MeSA, which was similar in magnitude to the MeSA released after Psm infection ( Figures 1B and 9A). By contrast, leaf MeSA emission from plants infected with the Pst cor 2 strain DB29 (Brooks et al, 2004) was only marginally elevated, falling by a factor of 60 below the amounts induced by wild-type Pst ( Figure 9A). Because coronatine functions as a virulence factor to promote bacterial multiplication in planta (Brooks et al, 2005), we comparatively determined the growth of (C) Leaf MeSA contents of Col-0 and bsmt1 mutant plants in response to inoculation with Psm avrRpm1 (gray bars), Psm (black bars), or infiltration with 10 mM MgCl 2 (white bars) at 24 HAI (means 6 SD, n = 3).…”

Section: Ja Signaling Regulates Mesa Production But Not Sarmentioning

confidence: 87%

“…It acts as a bacterial virulence factor that counteracts SA-dependent plant defense reactions by acting as a structural and functional mimic of bioactive jasmonates, most notably JA-Ile (Brooks et al, 2005;Thines et al, 2007;Katsir et al, 2008;Melotto et al, 2008). The availability of coronatine-deficient (cor 2 ) Pst mutants (Brooks et al, 2004) allowed us to test whether P. syringae-induced MeSA production would require the action of coronatine. Infection of Col-0 leaves with the coronatine-producing Pst wild-type strain evoked a strong emission of MeSA, which was similar in magnitude to the MeSA released after Psm infection ( Figures 1B and 9A).…”

Section: Ja Signaling Regulates Mesa Production But Not Sarmentioning

confidence: 99%

“…Pseudomonas syringae pv maculicola strain ES4326 (Psm), Psm carrying the avrRpm1 avirulence gene (Psm avrRpm1), P. syringae pv tomato DC3000 (Pst; strain KP105; Brooks et al, 2004), and Pst cor 2 (strain DB 29; Brooks et al, 2004) were grown in King's B medium containing the appropriate antibiotics at 288C. Overnight log phase cultures were washed three times with 10 mM MgCl 2 and diluted to different final optical densities for leaf inoculations.…”

Section: Cultivation Of Bacteriamentioning

confidence: 99%

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Methyl Salicylate Production and Jasmonate Signaling Are Not Essential for Systemic Acquired Resistance inArabidopsis

et al. 2009

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Systemic acquired resistance (SAR) develops in response to local microbial leaf inoculation and renders the whole plant more resistant to subsequent pathogen infection. Accumulation of salicylic acid (SA) in noninfected plant parts is required for SAR, and methyl salicylate (MeSA) and jasmonate (JA) are proposed to have critical roles during SAR long-distance signaling from inoculated to distant leaves. Here, we address the significance of MeSA and JA during SAR development in Arabidopsis thaliana. MeSA production increases in leaves inoculated with the SAR-inducing bacterial pathogen Pseudomonas syringae; however, most MeSA is emitted into the atmosphere, and only small amounts are retained. We show that in several Arabidopsis defense mutants, the abilities to produce MeSA and to establish SAR do not coincide. T-DNA insertion lines defective in expression of a pathogen-responsive SA methyltransferase gene are completely devoid of induced MeSA production but increase systemic SA levels and develop SAR upon local P. syringae inoculation. Therefore, MeSA is dispensable for SAR in Arabidopsis, and SA accumulation in distant leaves appears to occur by de novo synthesis via isochorismate synthase. We show that MeSA production induced by P. syringae depends on the JA pathway but that JA biosynthesis or downstream signaling is not required for SAR. In compatible interactions, MeSA production depends on the P. syringae virulence factor coronatine, suggesting that the phytopathogen uses coronatine-mediated volatilization of MeSA from leaves to attenuate the SA-based defense pathway.

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Section: Ja Signaling Regulates Mesa Production But Not Sarmentioning

confidence: 87%

Section: Ja Signaling Regulates Mesa Production But Not Sarmentioning

confidence: 99%

Section: Cultivation Of Bacteriamentioning

confidence: 99%

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Methyl Salicylate Production and Jasmonate Signaling Are Not Essential for Systemic Acquired Resistance inArabidopsis

et al. 2009

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“…Importantly, PR-1 is not hyperinduced in coi1-t, as observed after infection with P. syringae (Kloek et al, 2001) or Plectosphaerella cucumeria (Hernández-Blanco et al, 2007), to which coi1 is more resistant. In the P. syringae-Arabidopsis interaction, the increased resistance of coi1 is due to the lack of suppression of the SA pathway by the JA-Ile-mimic coronatine and was reverted to susceptibility after transformation with the NahG gene (Brooks et al, 2004;Laurie-Berry et al, 2006). Since a JA-Ile mimic influencing the V. longisporum-Arabidopsis interaction is unlikely (Fig.…”

Section: Coi1 In the Roots Influences The Disease Phenotype Of The Shootmentioning

confidence: 99%

The Vascular Pathogen Verticillium longisporum Requires a Jasmonic Acid-Independent COI1 Function in Roots to Elicit Disease Symptoms in Arabidopsis Shoots

et al. 2012

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Verticillium longisporum is a soil-borne vascular pathogen that causes reduced shoot growth and early senescence in Arabidopsis (Arabidopsis thaliana). Here, we report that these disease symptoms are less pronounced in plants that lack the receptor of the plant defense hormone jasmonic acid (JA), CORONATINE INSENSITIVE1 (COI1). Initial colonization of the roots was comparable in wild-type and coi1 plants, and fungal DNA accumulated to almost similar levels in petioles of wild-type and coi1 plants at 10 d post infection. Completion of the fungal life cycle was impaired in coi1, as indicated by the reduced number of plants with microsclerotia, which are detected on dead plant material at late stages of the disease. Contrary to the expectation that the hormone receptor mutant coi1 should display the same phenotype as the corresponding hormone biosynthesis mutant delayed dehiscence2 (dde2), dde2 plants developed wild-type-like disease symptoms. Marker genes of the JA and the JA/ethylene defense pathway were induced in petioles of wild-type plants but not in petioles of dde2 plants, indicating that fungal compounds that would activate the known COI1-dependent signal transduction chain were absent. Grafting experiments revealed that the susceptibility-enhancing COI1 function acts in the roots. Moreover, we show that the coi1-mediated tolerance is not due to the hyperactivation of the salicylic acid pathway. Together, our results have unraveled a novel COI1 function in the roots that acts independently from JA-isoleucine or any JA-isoleucine mimic. This COI1 activity is required for a yet unknown root-to-shoot signaling process that enables V. longisporum to elicit disease symptoms in Arabidopsis.

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“…Typically, the susceptibility phenotype of ios1-2 to Pst DC3000 is similar to the mutant bak1-5 (Supplemental Figure 2). We also evaluated the susceptibility of ios1 mutants to the Pst DC3000 hrcC -mutant, a strain defective in delivering type III effectors that cannot repress the PTI response, and consequently is mostly nonvirulent on Arabidopsis (Brooks et al, 2004). All three ios1 mutants tested allowed more growth of Pst DC3000 hrcC -than wild-type plants upon syringe infiltration (Supplemental Figure 3), suggesting a defective PTI response in ios1 mutants.…”

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confidence: 99%

Retraction

2015

The Plant Cell

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The authors of the above article request that it be retracted from The Plant Cell and issue the following statement:After publication of the article, we discovered irregularities and inappropriate data manipulation in Figure 6C produced by the first author Ching-Wei Chen from the Zimmerli laboratory. Specifically, the same blot image improperly appears twice in Figure 6, once in Figure 6A corresponding to the IP: a-GFP blot for FLS2-GFP and again in Figure 6C as IP: a-GFP for CERK1-GFP. We repeated these experiments but found that the original results associated with Figure 6C could not be replicated and instead suggest the potential for interaction between IOS1 and CERK1 in vivo in Nicotiana benthamiana. This raises questions about some of the conclusions of the article, and we feel the best course of action is to retract the article. We believe a major conclusion of the article remains unaffected, namely, that IOS1 is involved in the regulation of flg22-and elf18-triggered responses. However, we cannot rule out an additional role for IOS1 in mediating signaling by CERK1. We are undertaking follow-up experiments to verify the major findings and clarify the role of IOS1 in plant immunity signaling.www.plantcell.org/cgi/doi/10.1105/tpc.15.00374The Plant Cell, Vol. 27: 1563, May 2015 Plasma membrane-localized pattern recognition receptors (PRRs) such as FLAGELLIN SENSING2 (FLS2), EF-TU RECEPTOR (EFR), and CHITIN ELICITOR RECEPTOR KINASE1 (CERK1) recognize microbe-associated molecular patterns (MAMPs) to activate pattern-triggered immunity (PTI). A reverse genetics approach on genes responsive to the priming agent b-aminobutyric acid (BABA) revealed IMPAIRED OOMYCETE SUSCEPTIBILITY1 (IOS1) as a critical PTI player. Arabidopsis thaliana ios1 mutants were hypersusceptible to Pseudomonas syringae bacteria. Accordingly, ios1 mutants showed defective PTI responses, notably delayed upregulation of the PTI marker gene FLG22-INDUCED RECEPTOR-LIKE KINASE1, reduced callose deposition, and mitogen-activated protein kinase activation upon MAMP treatment. Moreover, Arabidopsis lines overexpressing IOS1 were more resistant to bacteria and showed a primed PTI response. In vitro pull-down, bimolecular fluorescence complementation, coimmunoprecipitation, and mass spectrometry analyses supported the existence of complexes between the membrane-localized IOS1 and BRASSINOSTEROID INSENSITIVE1-ASSOCIATED KINASE1 (BAK1)-dependent PRRs FLS2 and EFR, as well as with the BAK1-independent PRR CERK1. IOS1 also associated with BAK1 in a ligand-independent manner and positively regulated FLS2-BAK1 complex formation upon MAMP treatment. In addition, IOS1 was critical for chitinmediated PTI. Finally, ios1 mutants were defective in BABA-induced resistance and priming. This work reveals IOS1 as a novel regulatory protein of FLS2-, EFR-, and CERK1-mediated signaling pathways that primes PTI activation. INTRODUCTIONPlants possess multilayered recognition systems that detect pathogens at various stages of infection and proliferation. Recognition of m...

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Identification and Characterization of a Well-Defined Series of Coronatine Biosynthetic Mutants of Pseudomonas syringae pv. tomato DC3000

Cited by 213 publications

References 59 publications

Methyl Salicylate Production and Jasmonate Signaling Are Not Essential for Systemic Acquired Resistance inArabidopsis

Methyl Salicylate Production and Jasmonate Signaling Are Not Essential for Systemic Acquired Resistance inArabidopsis

The Vascular Pathogen Verticillium longisporum Requires a Jasmonic Acid-Independent COI1 Function in Roots to Elicit Disease Symptoms in Arabidopsis Shoots

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