Skip to main content
ARS Home » Midwest Area » Madison, Wisconsin » Vegetable Crops Research » Research » Publications at this Location » Publication #404422
Research Project: Management of Genetic Resources and Associated Information in the U. S. Potato Genebank

Location: Vegetable Crops Research

Title: Reproducible Quantitative Trait Loci for Resistance to Soft Rot Caused byDickeya dianthicola Derived from the Wild Potato Solanum microdontum(PI 458355) Are Located on Chromosomes 1, 3, and 5

Author
item Fenstemaker, Sean
item MA, XING - Cornell University
item Bamberg, John
item Swingle, Bryan

Submitted to: American Phytopathological Society
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/26/2023
Publication Date: 9/19/2023
Citation: Fenstemaker, S.M., Ma, X., Bamberg, J.B., Swingle, B.M. 2023. Reproducible Quantitative Trait Loci for Resistance to Soft Rot Caused byDickeya dianthicola Derived from the Wild Potato Solanum microdontum(PI 458355) Are Located on Chromosomes 1, 3, and 5. American Phytopathological Society. 114:580-589. https://doi.org/10.1094/PHYTO-05-23-0158-R.
DOI: https://doi.org/10.1094/PHYTO-05-23-0158-R

Interpretive Summary: Soft rot and blackleg bacterial diseases cost the potato industry millions of dollars in losses annually. Post-harvest tuber soft rot outbreaks especially devastates farmers who have invested in an entire crop-growing season. There have been increased outbreaks of soft rot in the US since 2014 caused by a highly virulent, nearly clonal bacterial strain of Dickeya dianthicola and there is an urgent need to develop resistant potato varieties. This work identifies resistant plants, describes the genetic basis of resistance soft rot, and provides new resources for developing disease-resistant potato varieties.

Technical Abstract: The potato crop wild relative Solanum microdontum is a breeder-friendly source of resistance to potato soft rot. We aimed to describe the genetic basis of resistance and develop molecular resources to improve introgression efforts. Our objectives were to: (1) identify loci associated with resistance in wild germplasm and (2) develop bi-parental populations in a self-compatible S. tuberosum genetic background to recover segregating F2 progenies, construct a linkage map, and identify quantitative trait loci (QTL). Under objective 1, tubers from 103 S. microdontum genotypes from the United States Potato Genebank were inoculated with a high virulence strain of Dickeya dianthicola, and lesion size was measured after a 24 h incubation period. Single-marker regression analysis was conducted using 3500 polymorphic Infinium array SNP markers. Regions on chromosomes 1, 2, 3, 5, 6, 9, and 12 were associated with resistance. S. microdontum accession PI 458355 was chosen as the donor parent. Under objective 2, PI 458355 was crossed with a highly fertile, self-compatible, diploid S. tuberosum pollen parent (PI 654351) to generate segregating F2 populations and validate chromosomal regions associated with resistance in S. microdontum germplasm. Three single S. microdontum (PI 458355) ' S. tuberosum (PI 654351) F1 plants were self-pollinated to generate 507 F2 progenies screened in subsequent evaluations, following the protocol under objective 1. Composite interval mapping was conducted using a genetic linkage map with 976 GBS-based SNP markers. Reproducible QTLs were detected on chromosomes 1, 3, and 5, explaining 12%, 14%, and 23% of the phenotypic variation, respectively. A homozygous S. microdontum allele is needed at the QTL on chromosome 3 in combination with heterozygous or homozygous S. microdontum alleles at QTLs on chromosomes 1 and 5 to significantly decrease lesion size compared to the homozygous S. tuberosum parent. The germplasm created in these studies provides a resource for studying traits from S. microdontum, and we can use the advanced F2 selections for future potato improvement.