Pseudomonas syringae
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.
Pseudomonas syringae is a member of the genus Pseudomonas, 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.
A phylogenomic analysis of 494 complete genomes from the entire Pseudomonas genus showed that P. syringae does not form a monophyletic species in the strict sense, but a wider evolutionary group that also included other species as well, such as P. avellanae, P. savastanoi, P. amygdali, and P. cerasi.
Pseudomonas 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.
Pseudomonas syringae also produces ice nucleation active proteins which cause water to freeze at fairly high temperatures, resulting in injury. 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.
Pseudomonas 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 the tomato, P. syringae has come to represent an important model system for experimental characterization of the molecular dynamics of plant-pathogen interactions.
History
In 1961, Paul Hoppe of the U.S. Department of Agriculture studied a corn fungus by grinding up infected leaves each season, then applying the powder to test corn for the following season to track the disease. A surprise frost occurred that year, leaving peculiar results. Only plants infected with the diseased powder incurred frost damage, leaving healthy plants unfrozen. This phenomenon baffled scientists until graduate student Steven E. Lindow of the University of Wisconsin–Madison with D.C. Arny and C. Upper found a bacterium in the dried leaf powder in the early 1970s. Steven E. Lindow, now a plant pathologist at the University of California, Berkeley, found that when this particular bacterium was introduced to plants where it is originally absent, the plants became very vulnerable to frost damage. He went on to identify the bacterium as P. syringae, investigate the role of P. syringae in ice nucleation and in 1977, discover the mutant ice-minus strain. He was later successful at producing the ice-minus strain of P. syringae through recombinant DNA technology, as well.Genomics
Based on a comparative genomic and phylogenomic analysis of 494 complete genomes from the entire Pseudomonas genus, P. syringae does not form a monophyletic species in the strict sense, but a wider evolutionary group that includes other species as well. The core proteome of the P. syringae group comprised 2944 proteins, whereas the protein count and GC content of the strains of this group ranged between 4973 and 6026 and between 58 and 59.3%, respectively.Disease cycle
Pseudomonas syringae overwinters on infected plant tissues such as regions of necrosis or gummosis but can also overwinter in healthy looking plant tissues. In the spring, water from rain or other sources will wash the bacteria onto leaves/blossoms where it will grow and survive throughout the summer. This is the epiphyte phase of P. syringae's life cycle where it will multiply and spread but will not cause a disease. Once it enters the plant through a leaf's stomata or necrotic spots on either leaves or woody tissue then the disease will start. The pathogen will then exploit and grow in intercellular space causing the leaf spots and cankers. P. syringae can also survive in temperatures slightly below freezing. These below freezing temperatures increase the severity of infection within trees like sour cherry, apricot, and peach.Epidemiology
Diseases caused by P. syringae tend to be favoured by wet, cool conditions—optimum temperatures for disease tend to be around, 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 P. 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 P. syringae is able to enter plants using its flagella and pili to swim towards a target host. It enters the plant via wounds of natural opening sites, as it is not able to breach the plant cell wall. An example of this is the partnership with the leaf-mining fly Scaptomyza flava, which creates holes in leaves during oviposition that the pathogen can take advantage of. The role of taxis in P. syringae has not been well-studied, but the bacteria are thought to use chemical signals released by the plant to find their host and cause infection.Overcoming host resistance
Effectors
Pseudomonas 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.Hop effectors
s are type III effectors which interfere with the Glycine max 2-hydroxyisoflavanone dehydratase. HopZ1b degrades daidzein after production, reducing concentrations and thus reducing the immunity it provides the plant.Phytotoxins
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.Elicitors
Pst DC3000 produces a PsINF1, the INF1 in P. syringae. Hosts respond with autophagy upon detection of this elicitor. Liu et al. 2005 finds this to be the only alternative to mass hypersensitivity leading to mass programmed cell death.Biofilm formation
Pseudomonas syringae produces polysaccharides which allow it to adhere to the surface of plant cells. It also releases quorum sensing molecules, which allows it to sense the presence of other bacterial cells nearby. If these molecules pass a threshold level, the bacteria change their pattern of gene expression to form a biofilm and begin expression of virulence-related genes. The bacteria secrete highly viscous compounds such as polysaccharides and DNA to create a protective environment in which to grow.Ice-nucleating properties
Pseudomonas 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 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, 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.Pseudomonas syringae has ina genes that make INA proteins which translocate to the outer bacterial membrane on the surface of the bacteria, where the proteins act as nuclei for ice formation. Artificial strains of P. syringae known as ice-minus bacteria have been created to reduce frost damage.
Pseudomonas syringae has been found in the center of hailstones, suggesting the bacterium may play a role in Earth's hydrological cycle.
Management
Currently there is not a 100% effective way to eradicate P. syringae from a field. The most common way to control this pathogen is to spray bactericides with copper compounds or other heavy metals that can be combined with fungicides or other pest control chemicals. Chemical treatments with fixed copper such as Bordeaux, copper hydroxide, and cupric sulfate are used to stop the spread of P. syringae by killing the bacteria while it is in the epiphyte stage on leaves, or woody parts of trees - however resistant P. syringae strains do exist. Spraying antibiotics such as streptomycin and organic bactericides is another way to control P. syringae but is less common than the methods listed above.New research has shown that adding ammonium nutrition to tomato plants can cause a metabolic change leading to resistance against Pseudomonas syringae. This "ammonium syndrome" causes nutrient imbalances in the plant and therefore triggers a defense response against the pathogen.
Strict hygiene practices used in orchards along with pruning in early spring and summer were proven to make the trees more resistant to P. syringae. Cauterizing cankers found on orchard trees can save the tree's life by stopping the infection from spreading.
Breeding plants for resistance is another somewhat effective way to avoid P. syringae. It has been successful in the cherry rootstock with Pseudomonas syringae pv. syringae, but so far, no other species are 100% resistant to this pathogen. Resistance breeding is a slow process, especially in trees. Unfortunately, P. syringae bacteria can adapt genetically to infect resistant plants, and the process for resistance breeding has to start over again.
A combination treatment of bacteriophage and carvacrol shows promise in control of both the planktonic and biofilm forms.