A Hitchhiker`s guide to the potato wart disease resistance galaxy

Charlotte Prodhomme, Gert van Arkel, Jarosław Plich, Jasper E. Tammes, Johan Rijk, Herman J. van Eck, Richard G. F. Visser & Jack H. Vossen

Theoretical and Applied Genetics December 2020; vol. 133:3419–3439.

Key message

Two novel major effect loci (Sen4 and Sen5) and several minor effect QTLs for potato wart disease resistance have been mapped. The importance of minor effect loci to bring full resistance to wart disease was investigated. Using the newly identified and known wart disease resistances, a panel of potato breeding germplasm and Solanum wild species was screened. This provided a state-of-the-art “hitch-hikers-guide” of complementary wart disease resistance sources.

Abstract

Potato wart disease, caused by the obligate biotrophic soil-born fungus Synchytrium endobioticum, is the most important quarantine disease of potato. Because of its huge impact on yield, the lack of chemical control and the formation of resting spores with long viability, breeding for resistant varieties combined with strict quarantine measures are the only way to efficiently and durably manage the disease. In this study, we set out to make an inventory of the different resistance sources. Using a Genome-Wide Association Study (GWAS) in the potato breeding genepool, we identified Sen4, associated with pathotypes 2, 6 and 18 resistance. Associated SNPs mapped to the south arm of chromosome 12 and were validated to be linked to resistance in one full-sib population. Also, a bulked segregant analysis combined with a Comparative Subsequence Sets Analysis (CoSSA) resulted in the identification of Sen5, associated with pathotypes 2, 6 and 18 resistance, on the south arm of chromosome 5. In addition to these two major effect loci, the GWAS and CoSSA allowed the identification of several quantitative trait loci necessary to bring full resistance to certain pathotypes. Panels of varieties and Solanum accessions were screened for the presence of Sen1, Sen2, Sen3, Sen4 and Sen5. Combined with pedigree analysis, we could trace back some of these genes to the ancestral resistance donors. This analysis revealed complementary resistance sources and allows elimination of redundancy in wart resistance breeding programs.

See: https://link.springer.com/article/10.1007/s00122-020-03678-x

Figure 1: GWAS performed on pathotypes 2, 6 and 18 resistance. Manhattan plots of the GWAS performed on a P2, b P6 and c P18 resistance. The x axis represents the 12 potato chromosomes. Markers from unanchored scaffolds (also referred to as Chr0), chloroplast and mitochondrion markers are indicated by U. The horizontal red line is the threshold of significance as calculated by the method of Li and Ji (2005). Significant markers above the threshold are highlighted in green. The markers from the Sen4 haplotype and from the chromosome 11 haplotype which is associated with resistance in the AxD, KxA and AxV populations are indicated. The SNP array was designed with an emphasis on 800 genes on gene rich arms and avoiding pericentromeric heterochromatin, which resulted in artificial peaks towards the end of the chromosomes (color figure online).