Pseudomonas viridiflava and P. syringae—Natural Pathogens of Arabidopsis thaliana

Jakob, Katrin; Goss, Erica M.; Araki, Hideki; Van, Tam T.; Kreitman, Martin; Bergelson, Joy

doi:10.1094/mpmi.2002.15.12.1195

Cited by 83 publications

(108 citation statements)

References 65 publications

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“…We were surprised to find a 390 single dominant Pseudomonas lineage in the study area, given that wild A. thaliana populations can be colonized 391 by a diversity of Pseudomonas pathogenic species (Jakob et al, 2002;Kniskern et al, 2011). We note, though, 392 that while the OTU5 strains share many genetic features, they are not functionally synonymous--instead they 393 are differentiated both at the level of gene content and the level of virulence.…”

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confidence: 90%

“…Arabidopsis thaliana is a globally distributed wild plant 64 capable of colonizing poor substrates as well as fertilised soils (Weigel, 2012). Arabidopsis thaliana populations 65 across the globe are hosts to Pseudomonas, and several of the most abundant Pseudomonas strains are 66 pathogenic on A. thaliana, even though they are likely not specialized on this species as a host (Barrett et al, 67 2011;Bodenhausen et al, 2014; Cai et al, 2011;Jakob et al, 2002Jakob et al, , 2007Kniskern et al, 2011). 68…”

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Stability of association betweenArabidopsis thalianaandPseudomonaspathogens over evolutionary time scales

Karasov

Almario

Friedemann

et al. 2018

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SummaryCrop disease outbreaks are often associated with clonal expansions of single pathogenic lineages. To determine 20 whether similar boom-and-bust scenarios hold for wild plant pathogens, we carried out a multi-year multi-site 21 survey of Pseudomonas in the natural host Arabidopsis thaliana. The most common Pseudomonas lineage 22 corresponded to a pathogenic clade present in all sites. Sequencing of 1,524 Pseudomonas genomes revealed 23 this lineage to have diversified approximately 300,000 years ago, containing dozens of genetically distinct 24 pathogenic sublineages. These sublineages have expanded in parallel within the same populations and are 25 differentiated both at the level of gene content and disease phenotype. Such coexistence of diverse sublineages 26indicates that in contrast to crop systems, no single strain has been able to overtake these A. thaliana 27 populations in the recent past. Our results suggest that the selective pressures acting on a plant pathogen in 28 wild hosts may be more complex than those in agricultural systems. 29 Introduction 30In agricultural and clinical settings, pathogenic colonizations are frequently associated with expansions of single 31 or a few genetically identical microbial lineages (Butler et al., 2013; Cai et al., 2011;Kolmer, 2005; Park et al., 32 2015;Stukenbrock and McDonald, 2008; Yoshida et al., 2013). The conditions that lead to such epidemics-such 33 as reduced host genetic diversity (Zhu et al., 2000), absence of competing microbial communities (Brown et al., 34 2013) or high transmission rates (Park et al., 2015)-are, however, by no means a universal feature of 35 pathogenic infections. Instead, many, if not most, pathogens can colonize host populations that are both 36 genetically diverse and that can accommodate a diversity of other microbes (Barrett et al., 2009; Falkinham et 37 al., 2015;Woolhouse et al., 2001). 38Factors that drive pathogen success in such more complex situations are less well understood than for 39 clonal epidemics. For example, if a pathogen species persists at high numbers in non-host environments, does 40 each host become infected by a different pathogen strain? Or does a multitude of genetically distinct pathogens 41 infect each host? And do different colonizing strains use disparate mechanisms to become established even 42 within genetically similar host individuals? The answers to these questions inform on how (and if) a host 43 population can evolve partial or even complete pathogen resistance (Anderson and May, 1982; Barrett et al., 44 2009; Karasov et al., 2014a;Laine et al., 2011). Several studies over the past 20 years have attempted to infer 45 the distributions of non-epidemic pathogens in both host and non-host environments (Falkinham et al., 2015; 46 Wiehlmann et al., 2007). These studies, which have observed a range of different patterns, are unfortunately 47 often limited to the historic strains that are available, and the conclusions vary for different collections, even of 48 the same pathogen ...

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Stability of association betweenArabidopsis thalianaandPseudomonaspathogens over evolutionary time scales

Karasov

Almario

Friedemann

et al. 2018

Preprint

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“…In a previous study, we identified two paralogous PAIs in P. viridiflava , a prevalent natural pathogen of A. thaliana ( Jakob et al 2002). Although these PAIs (T-and S-PAI, respectively) share 25 gene homologs, they are structurally distinct.…”

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Molecular Evolution of Pathogenicity-Island Genes in Pseudomonas viridiflava

et al. 2007

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The bacterial pathogen Pseudomonas viridiflava possesses two pathogenicity islands (PAIs) that share many gene homologs, but are structurally and phenotypically differentiated (T-PAI and S-PAI). These PAIs are paralogous, but only one is present in each isolate. While this dual presence/absence polymorphism has been shown to be maintained by balancing selection, little is known about the molecular evolution of individual genes on the PAIs. Here we investigate genetic variation of 12 PAI gene loci (7 on T-PAI and 5 on S-PAI) in 96 worldwide isolates of P. viridiflava. These genes include avirulence genes (hopPsyA and avrE ), their putative chaperones (shcA and avrF ), and genes encoding the type III outer proteins (hrpA, hrpZ, and hrpW ). Average nucleotide diversities in these genes (p ¼ 0.004-0.020) were close to those in the genetic background. Large numbers of recombination events were found within PAIs and a sign of positive selection was detected in avrE. These results suggest that the PAI genes are evolving relatively freely from each other on the PAIs, rather than as a single unit under balancing selection. Evolutionarily stable PAIs may be preferable in this species because preexisting genetic variation enables P. viridiflava to respond rapidly to natural selection.

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“…We investigate the generality of these changes in development by examining the effects of three distantly related pathogens: P. syringae and Xanthomonas campestris, which are biotrophic bacterial pathogens, and Peronospora parasitica, which is a biotrophic oomycete. All of these pathogens occur in natural Arabidopsis populations (Tsuji and Somerville, 1992;Holub et al, 1994;Jakob et al, 2002). We also address how the amount of pathogen in a plant affects development and whether R gene resistance affects developmental responses to pathogen infection.…”

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A Developmental Response to Pathogen Infection in Arabidopsis

2003

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We present evidence that susceptible Arabidopsis plants accelerate their reproductive development and alter their shoot architecture in response to three different pathogen species. We infected 2-week-old Arabidopsis seedlings with two bacterial pathogens, Pseudomonas syringae and Xanthomonas campestris, and an oomycete, Peronospora parasitica. Infection with each of the three pathogens reduced time to flowering and the number of aerial branches on the primary inflorescence. In the absence of competition, P. syringae and P. parasitica infection also increased basal branch development. Flowering time and branch responses were affected by the amount of pathogen present. Large amounts of pathogen caused the most dramatic changes in the number of branches on the primary inflorescence, but small amounts of P. syringae caused the fastest flowering and the production of the most basal branches. RPS2 resistance prevented large changes in development when it prevented visible disease symptoms but not at high pathogen doses and when substantial visible hypersensitive response occurred. These experiments indicate that phylogenetically disparate pathogens cause similar changes in the development of susceptible Arabidopsis. We propose that these changes in flowering time and branch architecture constitute a general developmental response to pathogen infection that may affect tolerance of and/or resistance to disease.One way that plants can respond to pathogen infection is through an induced resistance response called R gene resistance. When a plant has an R gene that confers resistance to an infecting pathogen, the plant initiates extensive biochemical and structural defense mechanisms, including the production of phytoalexins and pathogenesis-related proteins, the strengthening of cell walls, local cell death, and systemic acquired resistance (Dangl and Jones, 2001). Plants that are "susceptible," i.e. do not have R gene resistance to a particular pathogen strain, exhibit many defenses similar to R gene resistance, but are slower in their expression of these responses (Yang et al., 1997;Maleck et al., 2000). Like R gene-resistant plants, susceptible plants have increased levels of salicylic acid (SA; O'Donnell et al., 2001), cell death, and defense mechanisms characteristic of systemic acquired resistance (Glazebrook, 2001). In addition, infected, susceptible plants can exhibit increased levels of jasmonic acid (JA), auxin, and ethylene (Dong, 1998;Lund et al., 1998;O'Donnell et al., 2003).These responses of plants to pathogen infection bear some similarity to responses to abiotic stress. Both can involve cell death (Beers and McDowell, 2001), ethylene, SA, and JA (Wang et al., 2002) and cause changes in the expression of some of the same transcription factors (Chen et al., 2002). One way in which plants respond to abiotic stresses is to accelerate their transition to reproduction. Researchers have noted that plants flower faster in response to shade, overcrowding, low nutrients, drought, heat, and low light quality (Casal ...

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Pseudomonas viridiflava and P. syringae—Natural Pathogens of Arabidopsis thaliana

Cited by 83 publications

References 65 publications

Stability of association betweenArabidopsis thalianaandPseudomonaspathogens over evolutionary time scales

Stability of association betweenArabidopsis thalianaandPseudomonaspathogens over evolutionary time scales

Molecular Evolution of Pathogenicity-Island Genes in Pseudomonas viridiflava

A Developmental Response to Pathogen Infection in Arabidopsis

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