AbstractPseudomonas syringae pv. actinidiae (Psa) Biovar 3, a virulent, canker-inducing pathogen is an economic threat to the kiwifruit (Actinidia spp.) industry worldwide. The commercially grown diploid (2x) A. chinensis var. chinensis is more susceptible to Psa than tetraploid and hexaploid kiwifruit. However information on the genetic loci modulating Psa resistance in kiwifruit is not available. Here we report mapping of quantitative trait loci (QTLs) regulating tolerance to Psa in a diploid kiwifruit population, derived from a cross between an elite Psa-susceptible ‘Hort16A’ and a tolerant male breeding parent P1. Using high-density genetic maps and intensive phenotyping, we identified a single QTL for Psa tolerance on Linkage Group (LG) 27 of ‘Hort16A’ revealing 16-19% phenotypic variance and candidate alleles for susceptibility and tolerance at this loci. In addition, six minor QTLs were identified in P1 on distinct LGs, exerting 4-9% variance. Complete tolerance in the F1 population is attained by additive effects from ‘Hort16A’ and P1 QTLs providing evidence that divergent genetic pathways fend-off virulent Psa strain. Two different bioassays further identified new QTLs for tissue-specific responses to Psa. Transcriptome analysis of Psa-tolerant and susceptible genotypes in field revealed hallmarks of basal defense and provided candidate RNA-biomarkers for screening Psa tolerance.
Multiple quantitative trait loci contribute to resistance to bacterial canker incited by Pseudomonas syringae pv. actinidiae in kiwifruit (Actinidia chinensis)
