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Microbiota modulates plant health and appears as a promising lever to develop innovative, sustainable and eco-friendly agro-ecosystems. Key patterns of microbiota assemblages in plants have been revealed by an extensive number of studies based on taxonomic profiling by metabarcoding. However, understanding the functionality of microbiota is still in its infancy and relies on reductionist approaches primarily based on the establishment of representative microbial collections. In Arabidopsis thaliana, most of these microbial collections include one strain per OTU isolated from a limited number of habitats, thereby neglecting the ecological potential of genetic diversity within microbial species. With this study, we aimed at estimating the extent of genetic variation between strains within the most abundant and prevalent leaf-associated non-pathogenic bacterial species in A. thaliana located south-west of France. By combining a culture-based collection approach consisting of the isolation of more than 7,000 bacterial colonies with an informative-driven approach, we isolated 35 pure strains from eight non-pathogenic bacterial species. We detected significant intra-specific genetic variation at the genomic level and for growth rate in synthetic media. In addition, significant host genetic variation was detected in response to most bacterial strains in in vitro conditions, albeit dependent on the developmental stage at which plants were inoculated, with the presence of both negative and positive responses on plant growth. Our study provides new genetic and genomic resources for a better understanding of the plant-microbe ecological interactions at the microbiota level. We also highlight the need of considering genetic variation in both non-pathogenic bacterial species and A. thaliana to decipher the genetic and molecular mechanisms involved in the ecologically relevant dialog between hosts and leaf microbiota.

National audience

The emergence and re-emergence of plant pathogenic microorganisms are processes that imply perturbations in both host and pathogen ecological niches. Global change is largely assumed to drive the emergence of new etiological agents by altering the equilibrium of the ecological habitats which in turn places hosts more in contact with pathogen reservoirs. In this context, the number of epidemics is expected to increase dramatically in the next coming decades both in wild and crop plants. Under these considerations, the identification of the genetic variants underlying natural variation of resistance is a pre-requisite to estimate the adaptive potential of wild plant populations and to develop new breeding resistant cultivars. On the other hand, the prediction of pathogen's genetic determinants underlying disease emergence can help to identify plant resistance alleles. In the genomic era, whole genome sequencing combined with the development of statistical methods led to the emergence of Genome Wide Association (GWA) mapping, a powerful tool for detecting genomic regions associated with natural variation of disease resistance in both wild and cultivated plants. However, GWA mapping has been less employed for the detection of genetic variants associated with pathogenicity in microbes. Here, we reviewed GWA studies performed either in plants or in pathogenic microorganisms (bacteria, fungi and oomycetes). In addition, we highlighted the benefits and caveats of the emerging joint GWA mapping approach that allows for the simultaneous identification of genes interacting between genomes of both partners. Finally, based on co-evolutionary processes in wild populations, we highlighted a phenotyping-free joint GWA mapping approach as a promising tool for describing the molecular landscape underlying plant - microbe interactions.

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International audience; Pseudomonas syringae est agent phytopathogène-environnemental reconnu comme modèle remarquable. Nous avons isolé cette bactérie phytopathogène bien au-delà des zones d’agriculture, dans de nombreux substrats sur plusieurs continents constituant une collection unique au monde (>7000 souches). Une classification de cette bactérie intégrant toute la diversité et délimitant clairement les frontières est nécessaire. Les hybridations ADN/ADN et le séquençage de génomes trop lourds, les phénotypes peu fiables, et le concept de pathovar inopérant, nous conduisent à utiliser le typage MLST pour cette classification qui délimite actuellement 24 clades au sein d’au moins 14 phylogroupes. La robustesse du résultat est confirmée par les données de génomique. Pour chaque phylogroupe, les phénotypes reliés au pouvoir pathogène ont été caractérisés. A partir de ces données génotypiques et phénotypiques, les spécificités des phylogroupes ont été déterminées et un système de classification extensible à d’éventuels nouveaux groupes a été proposé. Un outil simple d’identification par analyse d’un seul gène de ménage est proposé (Berge et al. 2014). Grâce à la génomique comparative, nous avons développé des PCR spécifiques permettant l’identification au groupe P. syringae entier (Guilbaud et al.) et aux phylogroupes (Borschinger et al.) pour un crible moyen-débit de P. syringae permettant d’établir la structure des populations sur de nombreux échantillons. Cette classification nous permet d’aborder des questions sur l’écologie des agents phytopathogènes et leur stratégie d’adaptation dans différents environnements.

International audience; The rapid emergence of new bacterial diseases negatively affects both human health and agricultural productivity. Although the molecular mechanisms underlying these disease emergences are shared between human- and plant-pathogenic bacteria, not much effort has been made to date to understand disease emergences caused by plant-pathogenic bacteria. In particular, there is a paucity of information in the literature on the role of environmental habitats in which plant-pathogenic bacteria evolve and on the stress factors to which these microbes are unceasingly exposed. In this microreview, we focus on three molecular mechanisms underlying pathogenicity in bacteria, namely mutations, genomic rearrangements and the acquisition of new DNA sequences through horizontal gene transfer (HGT). We briefly discuss the role of these mechanisms in bacterial disease emergence and elucidate how the environment can influence the occurrence and regulation of these molecular mechanisms by directly impacting disease emergence. The understanding of such molecular evolutionary mechanisms and their environmental drivers will represent an important step towards predicting bacterial disease emergence and developing sustainable management strategies for crops.

Pseudomonas syringae est agent phytopathogène-environnemental reconnu comme modèle remarquable. Nous avons isolé cette bactérie phytopathogène bien au-delà des zones d’agriculture, dans de nombreux substrats sur plusieurs continents constituant une collection unique au monde (>7000 souches). Une classification de cette bactérie intégrant toute la diversité et délimitant clairement les frontières est nécessaire. Les hybridations ADN/ADN et le séquençage de génomes trop lourds, les phénotypes peu fiables, et le concept de pathovar inopérant, nous conduisent à utiliser le typage MLST pour cette classification qui délimite actuellement 24 clades au sein d’au moins 14 phylogroupes. La robustesse du résultat est confirmée par les données de génomique. Pour chaque phylogroupe, les phénotypes reliés au pouvoir pathogène ont été caractérisés.[br/] A partir de ces données génotypiques et phénotypiques, les spécificités des phylogroupes ont été déterminées et un système de classification extensible à d’éventuels nouveaux groupes a été proposé. Un outil simple d’identification par analyse d’un seul gène de ménage est proposé (Berge et al. 2014). Grâce à la génomique comparative, nous avons développé des PCR spécifiques permettant l’identification au groupe P. syringae entier (Guilbaud et al.) et aux phylogroupes (Borschinger et al.) pour un crible moyen-débit de P. syringae permettant d’établir la structure des populations sur de nombreux échantillons. [br/] Cette classification nous permet d’aborder des questions sur l’écologie des agents phytopathogènes et leur stratégie d’adaptation dans différents environnements.

National audience

International audience; The phyllosphere is known for hosting a great diversity of fungi, yeasts and bacteria. These microorganisms interact with each other and with the host plant in the form of symbiosis, mutualism, commensalism, parasitism, competition or simply neutralism. Pseudomonas syringae is a ubiquitous epiphytic bacterium commonly found in these microbial communities. The phylogeny complex of P. syringae comprises 13 phylogroups, containing strains that are well-known pathogens and strains that apparently have limited capacity as pathogens. Emblematic among the pathogens are P. syringae pv. syringae (Pss) and P. syringae pv. actinidiae (Psa) belonging respectively to phylogroups 2 and 1. Bacterial blights of fruit trees caused by P. syringae lead to significant economic losses worldwide. With the expansion of bacterial blight of kiwifruit caused by P. syringae pv. actinidiae and bacterial blight of apricot caused by P. syringae pv. syringae, the identification of reservoirs of these pathogenic strains and an understanding of the role of the accompanying diversity of P. syringae in disease epidemiology are needed. Here we describe the structure of P. syringae populations on orchard ground covers based on a series of PCR that specifically identify most of the phylogroups of this species. This efficient technique allows us to link population structure on ground covers to those associated with trees and to the botanical diversity and location of the ground cover reservoirs. The overall goal of these analyses are to identify microbiological contexts that are unfavorable for disease and to conceive management strategies of ground covers to foster these microbiological contexts.

National audience; Le chancre bactérien des arbres fruitiers causé par P. syringae engendre des pertes économiques importantes à l’échelle mondiale. Avec l’expansion du chancre du kiwi causé par P. s. pv. actinidiae (Psa) et le chancre de l’abricotier causé par P. s. pv. syringae (Pss), il est nécessaire d’identifier les réservoirs des souches pathogènes. L’un des réservoirs potentiels est le couvre-sol des vergers. Une solution pourrait être le développement de pratiques d’ingénierie écologique, plus précisément la gestion des couvre-sols dans le but de réduire leur impact en tant que source d’inoculum des maladies bactériennes des arbres fruitiers causées par P. syringae et augmenter leur rôle en tant que réserve de microorganismes antagonistes des pathogènes des arbres fruitiers. Cependant, avec la découverte récente de la complexité de la phylogénie de P. syringae et l’existence de phylogroupes renfermant plus de souches agressives que d’autres (Psa dans le phylogroupe 1, Pss dans le phylogroupe 2), l’un des premiers objectifs est le développement d’une méthode de détection spécifique, par PCR, permettant une identification rapide et précise des différents phylogroupes de P. syringae. Actuellement la seule méthode disponible est le séquençage de gènes spécifiques et conservés. La mise en application de cette nouvelle technique de génotypage permettrait l’analyse d’échantillons de grande taille. Cette technique pourrait également être utilisée en tant qu’outil de surveillance des champs et vergers. Effectivement, utiliser une technique ne ciblant qu’un seul pathovar peut être insuffisant sachant qu’il n’est pas rare d’avoir des espèces de plantes susceptibles à différentes souches de P. syringae. Ici seront présentés la mise au point de cette technique, ainsi qu’un exemple d’application concret (la structure des populations de P. syringae en vergers de kiwis).

National audience; Bacterial blight of fruit trees caused by Pseudomonas syringae causes significant economic losses worldwide. With the expansion of bacterial canker of kiwi caused by P. syringae pv. actinidiae (Psa) and bacterial canker of apricot caused by P. syringae pv. syringae (Pss), identification of reservoirs of pathogenic strains is required. One potential reservoir is ground covers in orchards. A solution could be the development of ecological engineering practices, particularly ground cover management in order to reduce their impact as a source of inoculum for bacterial diseases of fruit trees caused by P. syringae and increase their role as a reserve for microorganisms that are antagonistic to pathogens of fruit trees. However, with the recent discovery of the complexity of the phylogeny of P. syringae and the existence of phylogroups containing more aggressive strains than others (Psa in phylogroup 1, Pss in phylogroup 2), one of the first goals is the development of a specific molecular detection method, by PCR, allowing rapid and accurate identification of the different phylogroups of P. syringae. This would be much more efficient than the only method currently available - sequencing of specific conserved genes used in phylogenetic identification. The simple implementation of this new method of genotyping makes it possible to screen samples of very large size with little effort. This method can be deployed to develop methods of control of bacterial blight, and can be used as a generic mean of detecting and monitoring orchards and crops. Indeed, the use of a technique targeting a single pathovar may be insufficient, as it is not uncommon for plants to be simultaneously attacked by several different strains of P. syringae. The method of detection and identification of phylogroups will be presented and a concrete example for specific samples (ground cover, buds, twigs) from orchards of apricot and kiwi will be described.

International audience; Understanding ecology of pathogens like Pseudomonas syringae is central to addressing the complexity of disease emergence and pathogen evolution and to develop effective and sustainable methods of control. An indispensable prerequisite is a classification tool that represents as much of the diversity as possible and delimits accurately the boundaries. By adopting an intensive sampling strategy from several continents and multiple substrates within and beyond agricultural zones we made reliable phylogroup delimitation through multi-locus sequence typing (MLST). We identified 23 clades of P. syringae within 13 phylogroups among which the seven previously described were included. The robustness of MLST-phylogroups was confirmed by the phylogeny of the core genome of representative strains. We demonstrated that the citrate synthase (cts) housekeeping gene can accurately predict phylogenetic affiliation for more than 97 % of more than 700 strains and we proposed a list of cts sequences to be used as a simple tool for quickly and precisely classifying new strains. We therefore proposed an expandable framework mainly based on a broad database and cts genetic analysis into which more diversity can be integrated. Phenotypic traits rarely provided means for classification even if some combinations were highly probable in some phylogroups. However, by clarifying the classification of strains from a wide range of habitats and describing the genotypic and phenotypic profiles of the different phylogroups, we revealed a fascinating diversity of life histories and adapative strategies deployed within the P. syringae complex. This has led us to also develop specific genetic markers, one allowing the assignment of strains to the P. syringae complex at large and others to the individual phylogroups. Using these markers in simple, rapid, reliable and cheap multiplex PCR will allow a medium throughput screen of P. syringae strains leading to easy assessment of population structure in a wide range of samples.

International audience; Mutable bacterial cells are defective in their DNA repair system and they often have a phenotype different than their wild-type counterparts. In human bacterial pathogens, the mutable and hypermutable phenotype are often associated with general antibiotic resistance. Here, we quantified the occurrence of mutable cells in Pseudomonas viridiflava, a phytopathogenic bacterium in the P. syringae complex with a broad host range and capacity to live as saprophyte. Two phenotypic variants (transparent and mucoid) were produced by this bacterium. The transparent variant had a mutator phenotype, showed general antibiotic resistance and could not induce disease on the plant species tested (bean). In contrast, the mucoid variant did not display mutability nor resistance to antibiotics and was capable of inducing disease on bean. Both the transparent and mucoid variants were less fit when grown in vitro, while in planta both of the variants and wild-types attained similar population densities. Given the importance of the methyl-directed mismatch repair system (MMR) in the occurrence of mutable and hypermutable cells in human bacterial pathogens, we investigated whether mutations in mut genes were associated with mutator transparent cells in P. viridiflava. Our results showed no mutations in MMR genes in any of the P. viridiflava cells tested. Here we report that high mutation rate and antibiotic resistance are inversely correlated with pathogenicity in P. viridiflava but are not associated with mutations in MMR. In addition, P. viridiflava variants differ from variants produced by other phytopathogenic bacteria in the absence of reversion to the wild-type phenotype.

Understanding ecology of pathogens like Pseudomonas syringae is central to addressing the complexity of disease emergence and pathogen evolution and to develop effective and sustainable methods of control. An indispensable prerequisite is a classification tool that represents as much of the diversity as possible and delimits accurately the boundaries. By adopting an intensive sampling strategy from several continents and multiple substrates within and beyond agricultural zones we made reliable phylogroup delimitation through multi-locus sequence typing (MLST). We identified 23 clades of P. syringae within 13 phylogroups among which the seven previously described were included. The robustness of MLST-phylogroups was confirmed by the phylogeny of the core genome of representative strains. We demonstrated that the citrate synthase (cts) housekeeping gene can accurately predict phylogenetic affiliation for more than 97 % of more than 700 strains and we proposed a list of cts sequences to be used as a simple tool for quickly and precisely classifying new strains. We therefore proposed an expandable framework mainly based on a broad database and cts genetic analysis into which more diversity can be integrated. Phenotypic traits rarely provided means for classification even if some combinations were highly probable in some phylogroups. However, by clarifying the classification of strains from a wide range of habitats and describing the genotypic and phenotypic profiles of the different phylogroups, we revealed a fascinating diversity of life histories and adapative strategies deployed within the P. syringae complex. This has led us to also develop specific genetic markers, one allowing the assignment of strains to the P. syringae complex at large and others to the individual phylogroups. Using these markers in simple, rapid, reliable and cheap multiplex PCR will allow a medium throughput screen of P. syringae strains leading to easy assessment of population structure in a wide range of samples.

The phyllosphere is known for hosting a great diversity of fungi, yeasts and bacteria. These microorganisms interact with each other and with the host plant in the form of symbiosis, mutualism, commensalism, parasitism, competition or simply neutralism. Pseudomonas syringae is a ubiquitous epiphytic bacterium commonly found in these microbial communities. The phylogeny complex of P. syringae comprises 13 phylogroups, containing strains that are well-known pathogens and strains that apparently have limited capacity as pathogens. Emblematic among the pathogens are P. syringae pv. syringae (Pss) and P. syringae pv. actinidiae (Psa) belonging respectively to phylogroups 2 and 1. Bacterial blights of fruit trees caused by P. syringae lead to significant economic losses worldwide. With the expansion of bacterial blight of kiwifruit caused by P. syringae pv. actinidiae and bacterial blight of apricot caused by P. syringae pv. syringae, the identification of reservoirs of these pathogenic strains and an understanding of the role of the accompanying diversity of P. syringae in disease epidemiology are needed. Here we describe the structure of P. syringae populations on orchard ground covers based on a series of PCR that specifically identify most of the phylogroups of this species. This efficient technique allows us to link population structure on ground covers to those associated with trees and to the botanical diversity and location of the ground cover reservoirs. The overall goal of these analyses are to identify microbiological contexts that are unfavorable for disease and to conceive management strategies of ground covers to foster these microbiological contexts.

Bacterial blight of fruit trees caused by Pseudomonas syringae causes significant economic losses worldwide. With the expansion of bacterial canker of kiwi caused by P. syringae pv. actinidiae (Psa) and bacterial canker of apricot caused by P. syringae pv. syringae (Pss), identification of reservoirs of pathogenic strains is required. One potential reservoir is ground covers in orchards. A solution could be the development of ecological engineering practices, particularly ground cover management in order to reduce their impact as a source of inoculum for bacterial diseases of fruit trees caused by P. syringae and increase their role as a reserve for microorganisms that are antagonistic to pathogens of fruit trees. However, with the recent discovery of the complexity of the phylogeny of P. syringae and the existence of phylogroups containing more aggressive strains than others (Psa in phylogroup 1, Pss in phylogroup 2), one of the first goals is the development of a specific molecular detection method, by PCR, allowing rapid and accurate identification of the different phylogroups of P. syringae. This would be much more efficient than the only method currently available - sequencing of specific conserved genes used in phylogenetic identification. The simple implementation of this new method of genotyping makes it possible to screen samples of very large size with little effort. This method can be deployed to develop methods of control of bacterial blight, and can be used as a generic mean of detecting and monitoring orchards and crops. Indeed, the use of a technique targeting a single pathovar may be insufficient, as it is not uncommon for plants to be simultaneously attacked by several different strains of P. syringae. The method of detection and identification of phylogroups will be presented and a concrete example for specific samples (ground cover, buds, twigs) from orchards of apricot and kiwi will be described.

Pseudomonas syringae is a phytopathogenic bacterium that attacks both herbaceous and woody plants. In the last 20 years, more than 55 disease outbreaks caused by this bacterium have been reported on woody plants. The recent studies concerning the ecology of P. syringae demonstrated that this bacterium is present in several environmental habitats. These studies also showed that the environment is a reservoir of different P. syringae genetic lineages. In this thesis, I made an effort to understand what kind of evolutionary mechanisms can underline the emergence of new P. syringae pathogenic strains and how the environment can play a role in the evolution of pathogenicity traits of this bacterium. In particular, I focused on P. syringae lineages known to be pathogenic on kiwifruit. As a first step, I participated in a study about the diversity of P. syringae. This study was carried out in the laboratory of Cindy Morris at INRA of Avignon (France), where I performed almost all the experiments of the thesis. In the study concerning the P. syringae diversity, we showed that the genetic diversity (investigated on strains isolated from a wide range of substrates) of this species complex is wider than what was previously reported by considering only strains isolated from diseased crops. In fact, we found that P. syringae is composed by 13 phylogroups. In this thesis I showed that the phylogroup 7 and 8, also called as P. viridiflava, are formed by two different Type Three Secretion Systems. However, the evolution of these two systems does not seem to be related with the ability of P. viridiflava to cause disease. In addition I showed that avrE was the only effector correlated with the pathogenicity; it seems to be necessary but not sufficient for strains to be pathogenic. In the study concerning the role of the environment as reservoirs of P. syringae pathogenic to kiwifruit, we demonstrated that strains from aquatic habitats are kiwifruit pathogens since they are able to multiply into the kiwifruit tissues as well as cause the bacterial canker disease. These environmental strains, such as the strains that cause the bacterial canker of kiwifruit, have an operon for the degradation of phenolic compounds. We then hypothesized that this operon is important during the kiwifruit vascularization. In addition, we demonstrated that the environmental strains share 18 effectors with the epidemic strains but they lack 13 of the effectors present in all the epidemic strains. We then hypothesized that less aggressive environmental strains can acquire new effectors by horizontal gene transfer and become new future epidemic strains. This scenario, as I described in the review article, could be regulated by a defective methyl-directed repair system. The understanding of why this system can be defective could provide insights on the emergence of new diseases caused by P. syringae or other pathogens. Pseudomonas syringae é un batterio patogeno di piante erbacee e legnose. Negli ultimi 20 anni piantepiù di 55 nuove malattie causate da questo fitopatogeno sono state descritte. Dato che recenti studi sull’ecologia di P. syringae hanno messo in evidenza la sua ubiquità in differenti habitat ambientali, domande riguardati il ruolo dell’ambiente come “reservoire” di linee genetiche patogene di P. syringae sono rapidamente emerse negli ultimi cinque anni. In questa tesi é stato fatto uno sforzo per comprendere quali meccanismi evolutivi possono entrare in gioco nell’evoluzione di ceppi patogeni di P. syringae e su come l’ambiente in sensu latu possa essere coinvolto nell’evoluzione di tratti connessi con la patogenicità. In particolare mi sono focalizzata su linee genetiche di P. syringae conosciute essere patogene per l’ actinidia. Come primo passo nella mia ricerca ho collaborato ad un lavoro sulla diversità di P. syringae nel laboratorio di Cindy Morris, INRA di Avignone-France) in cui ho condotto la maggior parte delle mie ricerche di tesi. Nel lavoro riguardante la diversità di P. syringae, abbiamo messo in evidenza che le diversità conosciuta fino ad oggi, e basata su ceppi isolati da piante di origine agraria, é molto sottostimata. Analizzando ceppi provenienti da tutti gli ambienti abbiamo trovato che il complesso P. syringae é costituito da 13 gruppi genetici. Nella mia tesi, in particolare, ho messo in evidenza che il gruppo 7 e 8, costituiti da ciò che viene chiamato P. viridiflava, sono formati da due diversi Type Three Secretion System. L’evoluzione di questi due sistemi non sembra però essere connessa con l’abilità di P. viridiflava in indurre la malattia. Inoltre abbiamo messo in risalto che l’unico effettore connesso con la patogenicità é l’AvrE. Nel lavoro riguardante il ruolo dell’ambiente come “reservoire” di patogeni dell’actinidia abbiamo dimostrato che ceppi isolati da ambienti acquatici rappresentano patogeni deboli ma capaci di crescere e sopravvivere in piante di actinidia allo stesso modo di ceppi che sono attualmente responsabili dell’epidemia del cancro batterico. Questi ceppi ambientali, come tutti i ceppi che causano il cancro batterico, hanno un operone per la degradazione di sostanze fenoliche, e abbiamo ipotizzato che questi geni siano importanti nella vascolarizzazione in tutte le infezioni di piante legnose. Inoltre abbiamo dimostrato che i ceppi ambientali condividono 18 effettori con i ceppi dell’epidemia ma ne mancano 13. Abbiamo quindi proposto che ceppi meno aggressivi provenienti da differenti substrati possano acquisire tramite trasferimento orizzontale nuovi effettori e quindi diventare più aggressivi e essere i rappresentanti di nuove future epidemie. Questo scenario evolutivo, come ho descritto nell’articolo di sintesi riguardante i meccanismi di evoluzione di nuove malattie emergenti, potrebbe essere regolato da un sistema di riparazione del DNA (methyl-directed mismatch repair system) difettoso. Capire il perché questo sistema a volte non funziona bene ci potrebbe aiutare nel capire e nel controllare l’emergenza di nuove malattie causate da P. syringae ed altri patogeni. Dottorato di ricerca in Protezione delle piante

International audience

International audience; As a species complex, Pseudomonas syringae exists in both agriculture and natural aquatic habitats. P. viridiflava, a member of this complex, has been reported to be phenotypically largely homogenous. We characterized strains from different habitats, selected based on their genetic similarity to previously described P. viridiflava strains. We revealed two distinct phylogroups and two different kinds of variability in phenotypic traits and genomic content. The strains exhibited phase variation in phenotypes including pathogenicity and soft rot on potato. We showed that the presence of two configurations of the Type III Secretion System [single (S-PAI) and tripartite (T-PAI) pathogenicity islands] are not correlated with pathogenicity or with the capacity to induce soft rot in contrast to previous reports. The presence/absence of the avrE effector gene was the only trait we found to be correlated with pathogenicity of P. viridiflava. Other Type III secretion effector genes were not correlated with pathogenicity. A genomic region resembling an exchangeable effector locus (EEL) was found in S-PAI strains, and a probable recombination between the two PAIs is described. The ensemble of the variability observed in these phylogroups of P. syringae likely contributes to their adaptability to alternating opportunities for pathogenicity or saprophytic survival.