The Review of Symptoms Is a Component of the

Review

. 2014 Dec;240(half dozen):1149-65.

doi: 10.1007/s00425-014-2151-ten. Epub 2014 Aug 26.

The phytotoxin coronatine is a multifunctional component of the virulence armament of Pseudomonas syringae

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  • PMID: 25156488
  • PMCID: PMC4228168
  • DOI: ten.1007/s00425-014-2151-10

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Review

The phytotoxin coronatine is a multifunctional component of the virulence armament of Pseudomonas syringae

Xueqing Geng  et al. Planta. 2014 Dec .

Free PMC article

Abstract

Plant pathogens deploy an array of virulence factors to suppress host defense and promote pathogenicity. Numerous strains of Pseudomonas syringae produce the phytotoxin coronatine (COR). A major attribute of COR office is its ability to mimic a bioactive jasmonic acid (JA) cohabit and thus target the JA-receptor COR-insensitive ane (COI1). Biological activities of COR include stimulation of JA-signaling and consequent suppression of SA-dependent defense through combative crosstalk, antagonism of stomatal closure to allow bacterial entry into the interior of plant leaves, contribution to chlorotic symptoms in infected plants, and suppression of establish cell wall defense through perturbation of secondary metabolism. Hither, we review the virulence function of COR, including updates on these established activities as well as more recent findings revealing COI1-independent action of COR and shedding light on cooperative or redundant defense suppression betwixt COR and type Three effector proteins.

Figures

Fig. 1
Fig. ane

Roles of coronatine and type III effectors in modulating defense-related hormone signaling. (i) Roles of coronatine. Coronatine (COR) is composed of ii moieties: coronafacic acid (CFA) and coronamic acid (CMA) (Bough et al. 1999). One time COR moves into the constitute cell (presumably through diffusion), it activates JA-signaling through mimicking JA-amino acid conjugates such as (+)-seven-JA-isoleucine (JA-Ile) shown in the model. COR is able to interact with SCFCOI1 receptor complex with modestly higher affinity than JA-Ile (Sheard et al. ; Katsir et al. ; Fonseca et al. 2009b). Like JA-Ile, COR serves as 'molecular glue' between the receptor complex SCFCOI1 and the negative regulator JAZ protein (Sheard et al. 2010), and triggers the degradation of JAZ through 26S proteosomal-mediated pathway (Chini et al. ; Thines et al. 2007). Upon JAZ degradation, positive regulator TFs (e.g. MYC2, bHLH, and MYBs) are released from suppression, and activate JA-responsive genes (Wasternack and Hause 2013). MYC2 too regulates several NAC TFs that suppress SA accumulation through regulating SA-biosynthesis gene ICS1 and SA modifying gene BSMT1. These NAC TFs were also found to be required for stomatal reopening induced by COR (Zheng et al. 2012). In return, SA-activated, cytosolic NPR1 monomers suppress the JA-signaling pathway. COR's ability to contribute to chlorotic disease symptoms is also mediated through COI1 (Mecey et al. 2011). COR is able to suppress callose degradation through inhibiting an ET-dependent indole glucosinolate pathway where the part of COI1 is unknown (Geng et al. ; Millet et al. 2010). Perhaps the CMA moiety of COR mimics the ET precursor ACC, and interferes with ET product. Additionaly, COR perturbs auxin and ABA signaling which could potentially offset the brake of bacterial growth caused by flg22-induced suppression of auxin signaling (Navarro et al. 2006) or ABA-induced stomatal closure (Melotto et al. 2006), respectively. Whether COI1 is engaged in auxin and/or ABA perturbation is unknown. ii) Roles of blazon Three effectors. AvrB or COR, cooperatively with other T3Es and dependent on COI1, induce expression of an ET responsive factor—RAP2.half-dozen (He et al. 2004). HopZ1a acetylates JAZ proteins, causing them to go destabilized dependent on COI1, and restores virulence to a cor- mutant of Pto DC3000 (Jiang et al. 2013). HopX1 directly destabilizes JAZ proteins without a requirement for COI1, likely via its cysteine protease activity, and restores virulence to a cor- mutant of Pto DC3000. HopX1 shares additional activities with COR, including reopening of stomata, causing plant cells to lose chlorophyll, and induction of chlorosis in susceptible plants (Gimenez-Ibanez et al. 2014). HopM1 affects SA-dependent secretory pathway through interacting with and degrading an ARF-Gef family protein involved in vesicle trafficking called AtMIN7 (Nomura et al. 2006). HopM1 is also functionally redundant with COR in suppressing an SA-contained defense sector of which the mechanism is unknown (Geng et al. 2012). Solid lines indicate established interactions. Question marks indicate unknown mechanisms. Hormone/coronatine/effector-specifc functions are colour coded: bold orange lines coronatine-related functions, yellowish lines JA-related functions, greenish lines SA-related functions, bluish lines ET-related functions, blackness lines T3Es-related functions. Hormones are color coded, and indicated by solid circles. Type III effectors are color coded, and indicated by solid stars. Structural similarities betwixt compounds are indicated by aforementioned color shading of the respective chemical structures

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