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 p. s. pv. savastanoi, although as a result of dna-relatedness studies, it has been instated as a new species. it has three host-specific pathovars: p. s. fraxini (which causes ash canker), p. s. nerii (which attacks oleander), and p. s. oleae (which causes olive knot). determinants of host specificity a combination of the pathogen's effector genes and the plant's resistance genes is thought to determine which species a particular pathovar can infect. plants can develop resistance to a pathovar by recognising pathogen-associated molecular patterns (pamps) and launching an immune response. these pamps are necessary for the microbe to function, so cannot be lost, but 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 p. 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. pseudomonas 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 (hrp outer protein) 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 against it - that is, p. syringae pv. tomato dc3000 is able to infect a. thaliana - thus a. thaliana 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 is recognized by a. thaliana, any observed avr 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. examples of avr genes in p. syringae dc3000 and a. thaliana r-genes that recognize them avr genea. thaliana r-gene avrb rpm1 avrrpm1rpm1 avrrpt2 rps2 avrrps4rps4 avrrps6rps6 avrpphbrps5/resistance to pseudomonas syringae 5 (see also arabidopsis thaliana § rps5) the dynamin-related protein 2b/drp2b gene in a. thaliana is not directly an immunity gene, but by helping move external material into the intracellular network is indirectly related, and some mutants increase susceptibility. pseudomonas syringae pv. tomato strain dc3000, its derivatives, and its tomato host as its name suggests, p. syringae pv. tomato dc3000 (pst dc3000) is virulent to tomato (solanum lycopersicum). however, the tomato cultivar rio grande-ptor (rg-ptor), harboring the resistance gene pto, recognizes key effectors secreted by pst dc3000, making it resistant to the bacteria. studying the interactions between the pto-expressing tomato lines and pst dc3000 and its pathovars is a powerful system for understanding plant-microbe interactions. like other plants, the tomato has a two-tier pathogen defense system. the first and more universal line of plant defense, pattern-triggered immunity (pti), is activated when plant pattern recognition receptors (prrs) on the cell surface bind to pathogen-associated molecular patterns (pamps). the other branch of plant immunity, effector-triggered immunity (eti), is triggered when intracellular (nucleotide-binding site, leucine-rich repeat) nb-lrr proteins bind to an effector, a molecule specific to a particular pathogen. 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. 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. pst dc3000 has been modified to create the mutant strain pst dc3000∆avrpto∆avrptob (pst dc3000∆∆), which expresses neither avrpto nor avrptob. 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. 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. another useful dc3000 derivative is pst dc3000∆avrpto∆avrptob∆flic (pst dc3000∆∆∆). 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. by comparing plants within the same line that have been infected with either pst dc3000∆∆ or pst dc3000∆∆∆, researchers can determine if genes of interest are important to the flagellin recognition pathway of pti. by treating crispr-induced tomato knockout mutants (in a rg-ptor background) with pst dc3000, pst dc3000∆avrpto∆avrptob, or pst dc3000∆avrpto∆avrptob∆flic has led to the characterization of key components of the tomato immune system and continues to be used to further the field of tomato pathology. importance pseudomonas syringae has impacted many crop and orchard industries with its various pathovars. p. s. pv. actinidiae mesarich et al. 2017 provides several libraries for transposon insertion sequencing of mutants of p. s. a. the kiwifruit industry in new zealand has suffered catastrophic losses since their first known outbreak in 2007 from p. syringae pv. actinidiae. new zealand is second to italy in the total volume of kiwifruit exports making an annual revenue of $nz 1 billion, making it the most economically valuable export in the country. in 2014 the loss of exports alone was as high as nz$930 million. growers had to pay for treatments, and removal of infected vines along with suffering the loss of capital value in their orchards. for some, the orchard values went from nz$450,000/ha to $70,000/ha after the outbreak, which is the price of bare land. the total loss of equity for the country of new zealand was as high as nz$2 billion. between 2010 and 2012 over 2,000 hectares (4,900 acres) of italian kiwi orchards either were killed by p. syringae pv. actinidiae or were killed to contain the disease. the financial consequences for growers and their suppliers were severe, as were the economic consequences more widely.