Pseudomonas syringae

Pseudomonas syringae
Cultures of Pseudomonas syringae
Scientific classification
Kingdom:	Bacteria
Phylum:	Proteobacteria
Class:	Gamma Proteobacteria
Order:	Pseudomonadales
Family:	Pseudomonadaceae
Genus:	Pseudomonas
Species:	P. syringae
Binomial name
Pseudomonas syringae Van Hall, 1904
Type strain
ATCC 19310 CCUG 14279 CFBP 1392 CIP 106698 ICMP 3023 LMG 1247 NCAIM B.01398 NCPPB 281 NRRL B-1631
Pathovars
P. s. pv. aceris P. s. pv. aptata P. s. pv. atrofaciens P. s. pv. dysoxylis P. s. pv. japonica P. s. pv. lapsa P. s. pv. panici P. s. pv. papulans P. s. pv. pisi P. s. pv. syringae P. s. pv. morsprunorum

Pseudomonas syringae is a rod shaped, Gram-negative bacterium with polar flagella. It is a plant pathogen which can infect a wide range of plant species, and exists as over 50 different pathovars, all of which are available to researchers via international culture collections such as the NCPPB, ICMP, and others. It is unclear whether these pathovars represent a single species.

P. syringae is a member of the Pseudomonas genus, and based on 16S rRNA analysis, it has been placed in the P. syringae group.^[1] It is named after the lilac tree (Syringa vulgaris), from which it was first isolated.^[2]

P. syringae tests negative for arginine dihydrolase and oxidase activity, and forms the polymer levan on sucrose nutrient agar. Many but not all strains secrete the lipodepsinonapeptide plant toxin syringomycin,^[3] and it owes its yellow fluorescent appearance when cultured in vitro on King's B medium to production of the siderophore pyoverdin.^[4]

P. syringae also produce Ina proteins which cause water to freeze at fairly high temperatures, resulting in injury to plants. Since the 1970s, P. syringae has been implicated as an atmospheric "biological ice nucleator", with airborne bacteria serving as cloud condensation nuclei. Recent evidence has suggested that the species plays a larger role than previously thought in producing rain and snow. They have also been found in the cores of hailstones, aiding in bioprecipitation.^[5] These Ina proteins are also used in making artificial snow.^[6]

P. syringae pathogenesis is dependent on effector proteins secreted into the plant cell by the bacterial type III secretion system. Nearly 60 different type III effector families encoded by hop genes have been identified in P. syringae.^[7] Type III effectors contribute to pathogenesis chiefly through their role in suppressing plant defense. Owing to early availability of the genome sequence for three P. syringae strains and the ability of selected strains to cause disease on well-characterized host plants including Arabidopsis thaliana, Nicotiana benthemiana, and tomato, P. syringae has come to represent an important model system for experimental characterization of the molecular dynamics of plant-pathogen interactions.^{[citation needed]}

Bacterial speck on tomato in Upstate New York

Tomato plant leaf infected with bacterial speck

Ice nucleating properties

P. syringae, more than any mineral or other organism, is responsible for the surface frost damage in plants,^[8] exposed to the environment. For plants without antifreeze proteins, frost damage usually occurs between -4°C and -12°C as the water in plant tissue can remain in a supercooled liquid state. P. syringae can cause water to freeze at temperatures as high as −1.8 °C (28.8 °F),^[9] but strains causing ice nucleation at lower temperatures (down to −8°C) are more common.^[10] The freezing causes injuries in the epithelia and makes the nutrients in the underlying plant tissues available to the bacteria.^{[citation needed]}

P. syringae have ina (ice nucleation-active) genes that make Ina proteins which translocate to the outer bacterial membrane on the surface of the bacteria where the Ina proteins act as nuclei for ice formation.^[10] Artificial strains of P. syringae known as ice-minus bacteria have been created to reduce frost damage.

P. syringae have been found in the center of hailstones, suggesting that the bacterium may play a role in Earth's hydrological cycle.^[5]

Epidemiology

Disease by P. syringae tends to be favoured by wet, cool conditions—optimum temperatures for disease tend to be around 12–25°C, although this can vary according to the pathovar involved. The bacteria tend to be seed-borne, and are dispersed between plants via rain splash.^[11]

Although it is a plant pathogen, it can also live as a saprotroph in the phyllosphere when conditions are not favourable for disease.^[12] Some saprotrophic strains of P. syringae have been used as biocontrol agents against post-harvest rots.^[13]

Pathogenesis

A large number of P. syringae genes contribute to bacterial survival on and within the host plant, including those involved in bacterial attachment and nutrient uptake. This latter category may include siderophores, which are required for iron acquisition. The primary virulence factors produced by P. syringae are type III effectors and toxins.^{[citation needed]}

Type III Effectors

P. syringae Type III effectors, also known as Hop proteins, are coordinately synthesized by the bacterium in response to conditions inside the plant apoplast. Induction of the hop genes (also referred to by the older gene designation avr) is mediated by the ECF sigma factor HrpL. The effectors are injected into the plant cell by the bacterial type III secretion system. The first P. syringae type III effectors to be characterized were identified by their ability to cause a plant-type hypersensitive response upon recognition by plant resistance or R genes.^[14]

With the public release of complete genome sequences for three P. syringae strains it was possible to identify novel effector genes using conserved properties in the sequence. Useful properties for effector identification include the DNA motif to which HrpL binds, located upstream of the effector genes, as well as conserved elements in the amino acid sequences of the effector proteins involved in targeting them through the type III secretion system. Nearly 60 different type III effector families have been identified in P. syringae^[7] with selected individual strains encoding 30 or more. Gene names are assigned according to a nomenclature system that relies on both sequence and experimental characterization.^[15] Type III effectors contribute to pathogenesis chiefly through interference with diverse aspects of plant defense including formation of receptor complexes, MAP kinase signaling, vesicle transport, and RNA binding. A comprehensive listing of effector action in host plants can be found in the Gene Ontology-based P. syringae-Plant Interaction Resource.^[16] Ongoing sequencing of additional P. syringae strains is directed in large part to identifying correlations between effector repertoire and host range.

Toxins

Toxins contribute significantly to virulence in pathovars where they occur. The toxin coronatine suppresses salicylic acid-mediated defense as well as activating the jasmonic acid signaling pathway through mimicry of jasmonate. An important impact of coronatine action is to induce opening of the plant stoma to permit entry of the pathogen.^[17] Additional toxins characterized in P. syringae strains include syringomycin and syringopeptin, associated with attachment and surfactant activity and phaseolotoxin, tabtoxin, and mangotoxin which target metabolic pathways in the host.^[18]

Pathovars

Following ribotypical analysis, incorporation of several pathovars of Pseudomonas syringae into other species was proposed^[19] (see P. amygdali, 'P. tomato', P. coronafaciens, P. avellanae, 'P. helianthi', P. tremae, P. cannabina, and P. viridiflava). According to this schema, the remaining pathovars are as follows:

• Pseudomonas syringae pv. aceris attacks maple Acer species.
• Pseudomonas syringae pv. actinidiae attacks kiwifruit Actinidia deliciosa.^[20]
• Pseudomonas syringae pv. aesculi attacks horse chestnut Aesculus hippocastanum,^[21] causing Bleeding Canker of Horse Chestnut.
• Pseudomonas syringae pv. aptata attacks beets Beta vulgaris.
• Pseudomonas syringae pv. atrofaciens attacks wheat Triticum aestivum.
• Pseudomonas syringae pv. dysoxylis attacks the kohekohe tree Dysoxylum spectabile.
• Pseudomonas syringae pv. japonica attacks barley Hordeum vulgare.
• Pseudomonas syringae pv. lapsa attacks wheat Triticum aestivum.
• Pseudomonas syringae pv. panici attacks Panicum grass species.
• Pseudomonas syringae pv. papulans attacks crabapple Malus sylvestris species.
• Pseudomonas syringae pv. pisi attacks peas Pisum sativum.
• Pseudomonas syringae pv. syringae attacks Syringa, Prunus and Phaseolus species.

However, many of the strains for which new species groupings were proposed continue to be referred to in the scientific literature as pathovars of P. syringae, including pathovars tomato, phaseolicola, and maculicola. Note that Pseudomonas savastanoi was once considered a pathovar or sub-species of P. syringae, and in many places continues to be referred to as Pseudomonas syringae pv. savastanoi, although as a result of DNA-relatedness studies it has been instated as a new species.^[19] It itself has three host-specific pathovars: fraxini (which causes ash canker), nerii (which attacks oleander), and oleae (which causes olive knot).

Genome sequencing projects

The following table lists some of the genomes of strains of P. syringae that have been sequenced so far (or are in the process of being sequenced):

Pseudomonas syringae pv. tomato DC3000 (Donors reference DC52) is a mutant generated from NCPPB 1106. The difference between 1106 and DC3000 is rifampicin resistance (it was generated as a spontaneous mutant). Both DC3000 (NCPPB 4369) and NCPPB 1106 are available from the National Collection of Plant Pathogenic Bacteria.^{[citation needed]}

Pseudomonas syringae as a model system

Owing to early availability of genome sequences for Pseudomonas syringae pv tomato strain DC3000, P. syringae pv. syringae strain B728a, and P. syringae pv phaseolicola strain 1448A, together with the ability of selected strains to cause disease on well-characterized host plants such as Arabidopsis thaliana, Nicotiana benthamiana, and tomato, P. syringae has come to represent an important model system for experimental characterization of the molecular dynamics of plant-pathogen interactions.^[22] The P. syringae experimental system has been a source of pioneering evidence for the important role of pathogen gene products in suppressing plant defense. The nomenclature system developed for P. syringae effectors has been adopted by researchers characterizing effector repertoires in other bacteria,^[23] and methods used for bioinformatic effector identification have been adapted for other organisms. In addition, researchers working with P. syringae have played an integral role in the Plant-Associated Microbe Gene Ontology (PAMGO) working group, aimed at developing Gene Ontology terms that capture biological processes occurring during the interactions between organisms, and using the terms for annotation of gene products.^[24]

P. syringae pv tomato strain DC3000 and Arabidopsis thaliana

As mentioned above, the genome of P. syringae pv tomato DC3000 has been sequenced,^[25] and approximately 40 Hop (Hrp Outer Protein) effectors, pathogenic proteins that attenuate the host cell, have been identified.^[26] These 40 effectors are not recognized by A. thaliana thus making P. syringae pv tomato DC3000 virulent, that is, P. syringae pv tomato DC3000 is able to infect A. thaliana which is susceptible to this pathogen.

Many Gene-for-Gene relationships have been identified utilizing the two model organisms, P. syringae pv tomato strain DC3000 and Arabidopsis. The Gene-for-Gene relationship describes the recognition of pathogenic avirulence (avr) genes by host Resistance genes (R-genes). P. syringae pv tomato DC3000 is a useful tool for studying avr: R-gene interactions in A. thaliana because it can be transformed with aver genes from other bacterial pathogens, and furthermore, because none of the endogenous Hops are recognized by A. thaliana, thus any observed aver recognition identified utilizing this model can be attributed to recognition of the introduced aver by A. thaliana.^[27] The transformation of P. syringae pv tomato DC3000 with effectors from other pathogens have led to the identification of many R-genes in Arabidopsis to further advance knowledge of plant pathogen interactions.

See also

• Bioprecipitation
• Ice-minus bacteria
• Pseudomonas phage Φ6
• NCPPB

References

External links

• Lavín, José L; Kiil, Kristoffer; Resano, Ohiana; Ussery, David W; Oguiza, José A (2007). "Comparative genomic analysis of two-component regulatory proteins in Pseudomonas syringae". BMC Genomics 8: 397. doi:10.1186/1471-2164-8-397. PMC 2222644. PMID 17971244.