Exposure to Host Resistance Mechanisms Drives Evolution of Bacterial Virulence in Plants

Pitman, Andrew R.; Jackson, Robert W.; Mansfıeld, John W.; Kaitell, V.; Thwaites, Richard; Arnold, Dawn L.

doi:10.1016/j.cub.2005.10.074

Cited by 115 publications

(170 citation statements)

References 29 publications

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“…Similar results have been reported previously where an experimental evolution approach was used to investigate pathogen adaptation in completely unrelated environments such as mouse macrophage (Ensminger et al, 2012) and cystic fibrosis-like culture conditions in the presence and absence of fluoroquinolone antibiotics . In addition, unlike some other studies of the pathogen evolution in planta (Pitman et al, 2005;Lovell et al, 2009), our analysis did not detect the complete loss or gain of any gene among the bacterial strains compared with the parent.…”

contrasting

confidence: 93%

Host immune responses accelerate pathogen evolution

Trivedi

Wang

2013

The ISME Journal

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Pathogens face a hostile and often novel environment when infecting a new host, and adaptation is likely to be an important determinant of the success in colonization and establishment. We hypothesized that resistant hosts will impose stronger selection on pathogens than susceptible hosts, which should accelerate pathogen evolution through selection biased toward effector genes. To test this hypothesis, we conducted an experimental evolution study on Xanthomonas citri subsp. citri (Xcc) in a susceptible plant species and a resistant plant species. We performed 55 rounds of repeated reinoculation of Xcc through susceptible host grapefruit (isolates G1, G2, G3) and resistant host kumquat (isolates K1, K2, K3). Consequently, only K1 and K3 isolates lost their ability to elicit a hypersensitive response (HR) in kumquat. Illumina sequencing of the parental and descendant strains P, G1, G2, G3, K1, K2 and K3 revealed that fixed mutations were biased toward type three secretion system effectors in isolates K1 and K3. Parallel evolution was observed in the K1 and K3 strains, suggesting that the mutations result from selection rather than by random drift. Our results support our hypothesis and suggest that repeated infection of resistant hosts by pathogens should be prevented to avoid selecting for adaptive pathogens.

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contrasting

confidence: 93%

Host immune responses accelerate pathogen evolution

Trivedi

Wang

2013

The ISME Journal

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“…However, the coverage of scaffolds 43 and 100 within our Por 1_6 assembly is no different than that of the MLST genes in its own genome. Although we cannot rule out the presence of a low copy number plasmid, it is likely that Por 1_6 contains a plasmid integrated into the main genome, as noted for other P. syringae plasmids (Jackson et al 2000;Rohmer et al 2003;Pitman et al 2005).…”

Section: Por 1_ _6 Likely Harbors An Integrated Plasmidmentioning

confidence: 89%

De novo assembly using low-coverage short read sequence data from the rice pathogen Pseudomonas syringae pv. oryzae

Reinhardt¹,

Baltrus²,

Nishimura³

et al. 2008

Genome Res.

133

109

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We developed a novel approach for de novo genome assembly using only sequence data from high-throughput short read sequencing technologies. By combining data generated from 454 Life Sciences (Roche) and Illumina (formerly known as Solexa sequencing) sequencing platforms, we reliably assembled genomes into large scaffolds at a fraction of the traditional cost and without use of a reference sequence. We applied this method to two isolates of the phytopathogenic bacteria Pseudomonas syringae. Sequencing and reassembly of the well-studied tomato and Arabidopsis pathogen, Pto DC3000 , facilitated development and testing of our method. Sequencing of a distantly related rice pathogen, Por 1_6 , demonstrated our method's efficacy for de novo assembly of novel genomes. Our assembly of Por 1_6 yielded an N50 scaffold size of 531,821 bp with >75% of the predicted genome covered by scaffolds over 100,000 bp. One of the critical phenotypic differences between strains of P. syringae is the range of plant hosts they infect. This is largely determined by their complement of type III effector proteins. The genome of Por 1_6 is the first sequenced for a P. syringae isolate that is a pathogen of monocots, and, as might be predicted, its complement of type III effectors differs substantially from the previously sequenced isolates of this species. The genome of Por 1_6 helps to define an expansion of the P. syringae pangenome, a corresponding contraction of the core genome, and a further diversification of the type III effector complement for this important plant pathogen species.

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“…How can this requirement for precise functionality be reconciled with an additional role as receptors of the cognate effector proteins? Phytopathogenic bacteria evolve faster than plant hosts because of their higher mutation rates and shorter generation times; in addition, effector proteins are functionally redundant and therefore individually dispensable (Pitman et al, 2005). Furthermore, AvrPto and AvrPtoB are structurally unrelated; hence, recognition through the same subset of Pto residues provides an additional constraint to evolution.…”

Section: Discussionmentioning

confidence: 99%