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. It is named after the
lilac tree, from which it was first isolated.
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, and it owes
its yellow fluorescent appearance when cultured in vitro on King's B medium to
production of the siderophore pyoverdin. 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. These Ina
proteins are also used in making artificial snow.
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. 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 benthamiana, and tomato, P. syringae has come to represent an
important model system for experimental characterization of the molecular
dynamics of plant-pathogen interactions. 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 by rain splash. Although it is a plant pathogen, it can
also live as a saprotroph in the phyllosphere when conditions are not
favourable for disease. Some saprotrophic strains of P. syringae have
been used as biocontrol agents against postharvest rots.
Mechanisms of pathogenicity The mechanisms of Pseudomonas syringae
pathogenicity can be separated into several categories: ability to invade a
plant, ability to overcome host resistance, biofilm formation and
production of proteins with ice-nucleating properties.
= Ability to invade plants = Planktonic Pseudomonas syringae are able
to enter plants by using their flagella and pilli to swim towards a target host.
They enter the plant via wounds of natural opening sites, as they are not
able to breach the plant cell wall. The role of taxis in P. syringae has not
been well-studied, however it is thought that the bacteria use chemical signals
released by the plant to find their host and cause infection.
= Overcoming host resistance = P. syringae isolates carry a range of
virulence factors called type III secretion system effector proteins.
These proteins primarily function to cause disease symptoms and manipulate
the host's immune response to facilitate infection. The major family of T3SS
effectors in P. syringae is the hrp gene cluster, coding for the Hrp secretion
apparatus. The pathogens also produce phytotoxins
which injure the plant and can suppress the host immune system. One such
phytotoxin is coronatine, found in pathovars Pto and Pgl.
= Biofilm formation = P. syringae produce polysaccharides
which allow them to adhere to the surface of plant cells. They also
release quorum sensing molecules, which allow them to sense the presence of
other bacterial cells nearby. If these molecules pass a threshold level, the
bacteria will change their pattern of gene expression to form a biofilm and
begin expression virulence-related genes. The bacteria secrete highly
viscous compounds such as polysaccharides and DNA to create a
protective environment to grow in. = Ice-nucleating properties =
P. syringae—more than any mineral or other organism—is responsible for the
surface frost damage in plants 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, but
strains causing ice nucleation at lower temperatures are more common. The
freezing causes injuries in the epithelia and makes the nutrients in the
underlying plant tissues available to the bacteria.
P. syringae has ina 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. 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.
Pathovars Following ribotypical analysis,
incorporation of several pathovars of P. syringae into other species was
proposed. According to this schema, the remaining pathovars are:
Pseudomonas syringae pv. aceris attacks maple Acer species.
Pseudomonas syringae pv. actinidiae attacks kiwifruit Actinidia deliciosa.
Pseudomonas syringae pv. aesculi attacks horse chestnut Aesculus hippocastanum,
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. phaseolicola causes Halo blight of bean
Pseudomonas syringae pv. pisi attacks peas Pisum sativum.
Pseudomonas syringae pv. syringae attacks Syringa, Prunus and Phaseolus
species. Pseudomonas syringae pv. glycinea
attacks soybean Glycine max, causing Bacterial Blight of Soybean.
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. It has three host-specific
pathovars: fraxini, nerii, and oleae. = Determinants of host specificity =
It is thought that a combination of the pathogen's effector genes and the
plant's resistance genes determine which species a particular pathovar can
infect. Plants can develop resistance to a pathovar by recognising
pathogen-associated molecular patterns and launching an immune response. These
PAMPs are necessary for the microbe to function and therefore cannot be lost,
however the pathogen may find ways to suppress this immune response, leading
to an evolutionary arms race between the pathogen and the host.
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.
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, 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.
= P. syringae pv tomato strain DC3000 and Arabidopsis thaliana =
As mentioned above, the genome of P. syringae pv tomato DC3000 has been
sequenced, and approximately 40 Hop effectors, pathogenic proteins that
attenuate the host cell, have been identified. 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 genes by host resistance 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. 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 Di Lallo, G., Evangelisti, M., Mancuso,
F., Ferrante, P., Marcelletti, S., Tinari, A., ... & Thaller, M. C..
Isolation and partial characterization of bacteriophages infecting Pseudomonas
syringae pv. actinidiae, causal agent of kiwifruit bacterial canker. Journal of
basic microbiology. External links
Lavín, José L; Kiil, Kristoffer; Resano, Ohiana; Ussery, David W; Oguiza, José A.
"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.