出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2014/07/22 02:40:28」(JST)
Pseudomonas syringae | |
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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 |
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Type strain | |
ATCC 19310 CCUG 14279 |
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Pathovars | |
P. s. pv. aceris |
Pseudomonas syringae is a rod-shaped, Gram-negative bacterium with polar flagella. As a plant pathogen, it can infect a wide range of species, and exists as over 50 different pathovars, all of which are available to researchers from 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 produces 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 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]
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 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 has 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 has been found in the center of hailstones, suggesting the bacterium may play a role in Earth's hydrological cycle.[5]
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 by 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 postharvest rots.[13]
Following ribotypical analysis, incorporation of several pathovars of P. syringae into other species was proposed[14] (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:
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. Pseudomonas savastanoi was once considered a pathovar or subspecies 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.[14] It has three host-specific pathovars: fraxini (which causes ash canker), nerii (which attacks oleander), and oleae (which causes olive knot).
This 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):
Pathovar | Strain | Disease | Hosts |
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tomato | DC3000 (NCPPB 4369) | bacterial speck | tomato, Arabidopsis |
syringae | B728a | brown spot | bean |
phaseolicola | 1448A (NCPPB 4478) | halo blight | bean |
savastanoi | NCPPB 3335 | olive knot | olive |
tomato | T1 | bacterial speck | tomato |
tomato | NCPPB1108 | — | tomato |
tomato | Max13 | — | tomato |
tomato | K40 | — | tomato |
tabaci | ATCC11528 | wildfire | tobacco |
aesculi | 2250 | bleeding canker | European horse chestnut |
aesculi | NCPPB 3681 | leaf spot | Indian horse chestnut |
oryzae | 1_6 | — | rice |
syringae | FF5 | — | — |
syringae | 642 | — | — |
glycinea | race 4 | bacterial blight | soybean |
glycinea | B076 | bacterial blight | soybean |
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]
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.[17] 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,[18] 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 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.[19]
As mentioned above, the genome of P. syringae pv tomato DC3000 has been sequenced,[20] and approximately 40 Hop (Hrp Outer Protein) effectors, pathogenic proteins that attenuate the host cell, have been identified.[21] 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 using 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 avr genes from other bacterial pathogens, and furthermore, because none of the endogenous hops genes are recognized by A. thaliana, thus any observed aver recognition identified using this model can be attributed to recognition of the introduced avr by A. thaliana.[22] 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.
Examples of avr genes in Pseudomonas syringae DC3000 and A. thaliana R-genes that recognize them | |
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Avr gene | A. thaliana R-gene |
AvrB | RPM1 |
AvrRpm1 | RPM1 |
AvrRpt2 | RPS2 |
AvrRps4 | RPS4 |
AvrRps6 | RPS6 |
AvrPphB | RPS5 |
Di Lallo, G., Evangelisti, M., Mancuso, F., Ferrante, P., Marcelletti, S., Tinari, A., ... & Thaller, M. C. (2014). Isolation and partial characterization of bacteriophages infecting Pseudomonas syringae pv. actinidiae, causal agent of kiwifruit bacterial canker. Journal of basic microbiology.
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リンク元 | 「シリンゲ菌」「シュードモナス・シリンゲ」「P. syringae」 |
関連記事 | 「syring」「Pseudomonas」 |
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