AI Article Synopsis

  • Pseudomonas syringae causes significant diseases in fruit trees, particularly apricot bacterial canker, which is hard to control due to limited preventive measures and unclear genetic resistance patterns.
  • Researchers conducted a four-year study on 73 apricot accessions, measuring their susceptibility to canker through artificial inoculations and employing genome-wide association study methods to analyze genetic factors linked to resistance.
  • The study identified 11 significant associations across 7 key loci, highlighting two major loci on chromosomes 5 and 6 that explain a large portion of the phenotypic variance, suggesting co-adaptive genetic strategies in response to environmental selection pressures.

Article Abstract

Background: Diseases caused by Pseudomonas syringae (Ps) are recognized as the most damaging factors in fruit trees with a significant economic and sanitary impact on crops. Among them, bacterial canker of apricot is exceedingly difficult to control due to a lack of efficient prophylactic measures. Several sources of partial resistance have been identified among genetic resources but the underlying genetic pattern has not been elucidated thus far. In this study, we phenotyped bacterial canker susceptibility in an apricot core-collection of 73 accessions over 4 years by measuring canker and superficial browning lengths issued from artificial inoculations in the orchard. In order to investigate the genetic architecture of partial resistance, we performed a genome-wide association study using best linear unbiased predictors on genetic (G) and genetic x year (G × Y) interaction effects extracted from linear mixed models. Using a set of 63,236 single-nucleotide polymorphism markers genotyped in the germplasm over the whole genome, multi-locus and multi-variate mixed models aimed at mapping the resistance while controlling for relatedness between individuals.

Results: We detected 11 significant associations over 7 candidate loci linked to disease resistance under the two most severe years. Colocalizations between G and G × Y terms indicated a modulation on allelic effect depending on environmental conditions. Among the candidate loci, two loci on chromosomes 5 and 6 had a high impact on both canker length and superficial browning, explaining 41 and 26% of the total phenotypic variance, respectively. We found unexpected long-range linkage disequilibrium (LD) between these two markers revealing an inter-chromosomal LD block linking the two underlying genes. This result supports the hypothesis of a co-adaptation effect due to selection through population demography. Candidate genes annotations suggest a functional pathway involving abscisic acid, a hormone mainly known for mediating abiotic stress responses but also reported as a potential factor in plant-pathogen interactions.

Conclusions: Our study contributed to the first detailed characterization of the genetic determinants of partial resistance to bacterial canker in a Rosaceae species. It provided tools for fruit tree breeding by identifying progenitors with favorable haplotypes and by providing major-effect markers for a marker-assisted selection strategy.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6341767PMC
http://dx.doi.org/10.1186/s12870-019-1631-3DOI Listing

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