Title : Dissecting the polygenic basis of Psa resistance in tetraploid kiwifruit
Abstract:
Bacterial canker, caused by Pseudomonas syringae pv. actinidiae (Psa), has been one of the most destructive diseases affecting kiwifruit (Actinidia spp.) worldwide for over a decade. Despite ongoing breeding efforts, no fully resistant cultivars have yet been released, and disease management still relies mainly on preventive strategies and the cultivation of less susceptible genotypes. Nevertheless, some Actinidia species, particularly A. arguta, exhibit notable tolerance to the pathogen, making them valuable genetic resources for resistance breeding.
To dissect the genetic basis of Psa resistance, an interspecific tetraploid population derived from a cross between A. chinensis var. chinensis (susceptible) and A. arguta (tolerant) was evaluated under controlled infection conditions. Cane inoculations were performed, and lesion development was monitored for six weeks. Disease severity was quantified by measuring lesion length and infection rate. Genotyping was carried out using ddRAD sequencing, allowing the construction of a high-resolution interspecific linkage map. QTL analysis revealed several loci associated with resistance on chromosomes 4, 17, and 28, with the region on chromosome 28 showing a stronger effect on the resistance phenotype. A susceptibility-related QTL was also identified on chromosome 9.
In parallel, RNA-seq analysis of infected subcortical tissues from both parental genotypes uncovered differentially expressed genes associated with resistance and susceptibility responses. Together, these findings shed light on the polygenic nature of Psa resistance in kiwifruit and provide a genomic framework for developing resistant cultivars through marker-assisted selection.
