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Templeton, K.

Publications and source records attributed to Templeton, K..

2 recordsLinked to original sources

NbPTR1 confers resistance against Pseudomonas syringae pv. actinidiae in kiwifruit

Pseudomonas syringae pv. actinidiae biovar 3 (Psa3) causes a devastating canker disease in yellow-fleshed kiwifruit (Actinidia chinensis). The effector HopZ5, which is present in all isolates of Psa3 causing global outbreaks of pandemic kiwifruit canker disease, triggers immunity in Nicotiana benthamiana and is not recognised in susceptible A. chinensis cultivars. In a search for N. benthamiana non-host resistance genes against HopZ5, we found that the nucleotide-binding leucine-rich repeat receptor NbPTR1 recognised HopZ5. RPM1-interacting protein 4 (RIN4) orthologues from multiple plants, including kiwifruit, were associated with NbPTR1-mediated autoimmunity suppression and recognition of HopZ5. No functional orthologues of NbPTR1 were found in A. chinensis. NbPTR1 transformed into Psa3-susceptible A. chinensis var. chinensis Hort16A plants introduced HopZ5-specific resistance against Psa3. Altogether, this study suggested that expressing NbPTR1 in Psa3-susceptible kiwifruit is a viable approach to acquiring resistance to Psa3 and it provides valuable information for engineering resistance in otherwise susceptible kiwifruit genotypes.

plant biology↗

Multiple quantitative trait loci contribute tolerance to bacterial canker incited by Pseudomonas syringae pv. actinidiae in kiwifruit (Actinidia chinensis)

Pseudomonas 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.

plant biology↗