As a plant pathogen, it can infect a wide range of species, and exists as over 50 different pathovars,[2] all of which are available to researchers from international culture collections such as the NCPPB, ICMP, and others.

[5] 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,[6] and it owes its yellow fluorescent appearance when cultured in vitro on King's B medium to production of the siderophore pyoverdin.

[7] Pseudomonas syringae also produces ice nucleation active (INA) proteins which cause water (in plants) to freeze at fairly high temperatures (−1.8 to −3.8 °C (28.8 to 25.2 °F)), resulting in injury.

[8] 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.

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.

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.

Once it enters the plant through a leaf's stomata or necrotic spots on either leaves or woody tissue then the disease will start.

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.

[22] 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.

[21] Pseudomonas syringae isolates carry a range of virulence factors called type III secretion system (T3SS) effector proteins.

These proteins primarily function to cause disease symptoms and manipulate the host's immune response to facilitate infection.

The bacteria secrete highly viscous compounds such as polysaccharides and DNA to create a protective environment in which to grow.

[27] The freezing causes injuries in the epithelia and makes the nutrients in the underlying plant tissues available to the bacteria.

[citation needed] Pseudomonas syringae has been found in the center of hailstones, suggesting the bacterium may play a role in Earth's hydrological cycle.

[28] Spraying antibiotics such as streptomycin and organic bactericides is another way to control P. syringae but is less common than the methods listed above.

[29] New research has shown that adding ammonium (NH4+) nutrition to tomato plants can cause a metabolic change leading to resistance against Pseudomonas syringae.

[30] 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.

A combination treatment of bacteriophage and carvacrol shows promise in control of both the planktonic and biofilm forms.

Pseudomonas savastanoi was once considered a pathovar or subspecies of P. syringae, and in many places continues to be referred to as P. s. pv.

Plants can develop resistance to a pathovar by recognising pathogen-associated molecular patterns (PAMPs) and launching an immune response.

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.

[39] The P. syringae experimental system has been a source of pioneering evidence for the important role of pathogen gene products in suppressing plant defense.

ETI is generally more severe than PTI, and when a threshold of defense activation is reached, it can trigger a hypersensitive response (HR), which is purposeful death of host tissue to prevent the spread of infection.

[52] Two key effectors secreted by Pst DC3000 are AvrPto and AvrPtoB, which initiate ETI by binding the Pto/Prf receptor complex in Pto-expressing tomato lines like RG-PtoR.

By infecting RG-PtoR with Pst DC3000∆∆, ETI to the pathogen is not triggered due to the absence of the main effectors recognized by the Pto/Prf complex.

[54][55] In the lab this is highly valuable, as using Pst DC3000∆∆ allows researchers to study the function of PTI-candidate genes in RG-PtoR, which would otherwise be masked by ETI.

Like Pst DC3000∆∆, this strain does not express AvrPto and AvrPtoB, but it also has an additional knock-out for fliC, the gene encoding flagellin, whose fragments serve as main PAMPs required for tomato PTI.

[60] Growers had to pay for treatments, and removal of infected vines along with suffering the loss of capital value in their orchards.