"The work suggested that resistance arises from a relatively large number of sites, each with relatively minor effects. For example, the sites in the genome identified by quantitative trait analysis typically boosted resistance by about 10 points on the researchers' 100-point scale. In the genome-wide analysis, 17 individual genetic differences were associated with about a quarter of the heritable resistance traits."
"The researchers also took an alternative approach to identify resistance factors, comparing 100 chemicals produced by resistant and susceptible strains. Among the 41 chemicals detected at higher levels in the Chinese chestnut, the researchers found a metabolite, lupeol, that completely suppressed the growth of the fungal pathogen. Another, erythrodiol, limited its growth. If we can identify the genes involved in producing those chemicals, we could use that knowledge to guide directed breeding programs-or even engage in gene editing to increase their production."
Highest-quality chestnut genomes for American and Chinese species were completed, identifying about 25,000–30,000 genes in different assemblies. Quantitative trait locus mapping and genome-wide association analyses identified genomic regions associated with resistance and estimated effect sizes. Blight resistance appears polygenic, arising from many sites with relatively small effects; QTL-identified sites typically increased resistance by about 10 points on a 100-point scale, and 17 variants explained roughly one quarter of heritable resistance. Root rot resistance appears oligogenic, with a limited number of alleles having large impacts. Chemical profiling identified lupeol and erythrodiol as metabolites that strongly suppress the fungal pathogen, suggesting breeding or gene-editing targets.
Read at Ars Technica
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