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Quantitative trait loci for partial resistance to Pseudomonas syringae pv. maculicola in Arabidopsis thaliana.

ABSTRACT: Segregation of partial resistance to Pseudomonas syringae pv. maculicola (Psm) ES4326 was studied in the recombinant inbred population created from accessions (ecotypes) Columbia (Col-4), the more susceptible parent, and Landsberg (Ler-0). Plants were spray inoculated with lux-transformed bacteria in experiments to measure susceptibility. The amount of disease produced on a range of Col × Ler lines by spray inoculation was highly correlated with that produced by pressure infiltration of bacteria into the apoplast. Quantitative trait locus (QTL) analysis identified four loci that contributed to partial resistance: QRpsJIC-1.1, QRpsJIC-2.1, QRpsJIC-3.1 and QRpsJIC-5.1 on chromosomes 1, 2, 3 and 5, respectively. QRpsJIC-3.1, located 8.45 cM from the top of the consensus genetic map of chromosome 3, had a large, approximately additive effect on partial resistance, explaining 50% of the genetic variation in this population. Fine mapping narrowed the region within which this QTL was located to 62 genes. A list of candidate genes included several major classes of resistance gene.

SUBMITTER: Rant JC

PROVIDER: S-EPMC3902988 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Virulence of the phytopathogen Pseudomonas syringae pv. maculicola is rpoN dependent.

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The Genetic Network Controlling the Arabidopsis Transcriptional Response to Pseudomonas syringae pv. maculicola

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Housekeeping gene sequencing and multilocus variable-number tandem-repeat analysis to identify subpopulations within Pseudomonas syringae pv. maculicola and Pseudomonas syringae pv. tomato that correlate with host specificity.

Project description:Pseudomonas syringae pv. maculicola causes bacterial spot on Brassicaceae worldwide, and for the last 10 years severe outbreaks have been reported in the Loire Valley, France. P. syringae pv. maculicola resembles P. syringae pv. tomato in that it is also pathogenic for tomato and causes the same types of symptoms. We used a collection of 106 strains of P. syringae to characterize the relationships between P. syringae pv. maculicola and related pathovars, paying special attention to P. syringae pv. tomato. Phylogenetic analysis of gyrB and rpoD gene sequences showed that P. syringae pv. maculicola, which causes diseases in Brassicaceae, forms six genetic lineages within genomospecies 3 of P. syringae strains as defined by L. Gardan et al. (Int. J. Syst. Bacteriol. 49[Pt 2]:469-478, 1999), whereas P. syringae pv. tomato forms two distinct genetic lineages. A multilocus variable-number tandem-repeat (VNTR) analysis (MLVA) conducted with eight minisatellite loci confirmed the genetic structure obtained with rpoD and gyrB sequence analyses. These results provide promising tools for fine-scale epidemiological studies on diseases caused by P. syringae pv. maculicola and P. syringae pv. tomato. The two pathovars had distinct host ranges; only P. syringae pv. maculicola strains were pathogenic for Brassicaceae. A subpopulation of P. syringae pv. maculicola strains that are pathogenic for Pto-expressing tomato plants were shown to lack avrPto1 and avrPtoB or to contain a disrupted avrPtoB homolog. Taking phylogenetic and pathological features into account, our data suggest that the DC3000 strain belongs to P. syringae pv. maculicola. This study shows that P. syringae pv. maculicola and P. syringae pv. tomato appear multiclonal, as they did not diverge from a single common ancestral group within the ancestral P. syringae genomospecies 3, and suggests that pathovar specificity within P. syringae may be due to independent genetic events.

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