Genome-Wide Association Mapping Identifies Novel Loci for Quantitative Resistance to Blackleg Disease in Canola

Abstract

Blackleg disease, caused by the fungal pathogen Leptosphaeria maculans , continues to be a major concern for sustainable production of canola ( Brassica napus L.) in many parts of the world. The deployment of effective quantitative resistance (QR) is recognized as a durable strategy in providing natural defense to pathogens. Herein, we uncover loci for resistance to blackleg in a genetically diverse panel of canola accessions by exploiting historic recombination events which occurred during domestication and selective breeding by genome-wide association analysis (GWAS). We found extensive variation in resistance to blackleg at the adult plant stage, including for upper canopy infection. Using the linkage disequilibrium and genetic relationship estimates from 12,414 high quality SNPs, GWAS identified 59 statistically significant and “suggestive” SNPs on 17 chromosomes of B. napus genome that underlie variation in resistance to blackleg, evaluated under field and shade-house conditions. Each of the SNP association accounted for up to 25.1% of additive genetic variance in resistance among diverse panel of accessions. To understand the homology of QR genomic regions with Arabidopsis thaliana genome, we searched the synteny between QR regions with 22 ancestral blocks of Brassicaceae. Comparative analyses revealed that 25 SNP associations for QR were localized in nine ancestral blocks, as a result of genomic rearrangements. We further showed that phenological traits such as flowering time, plant height, and maturity confound the genetic variation in resistance. Altogether, these findings provided new insights on the complex genetic control of the blackleg resistance and further expanded our understanding of its genetic architecture.

Genetic Variance for Fusarium Crown Rot Tolerance in Durum Wheat

“…Whilst we have not investigated the genetic or physiological basis of FCR tolerance, it appears most likely a polygenic trait, similar to horizontal resistance to blackleg disease of canola (Salisbury et al 1995; Raman et al 2013). Similar to reports of effects of other plant traits on impact of FCR on yield, horizontal resistance to blackleg also appears to be a tolerance trait and it is confounded by other plant traits, such as flowering time, plant height and maturity (Raman et al 2020). Development of horizontal resistance to blackleg by repeated selection under heavy disease pressure (e.g.…”

“…Development of horizontal resistance to blackleg by repeated selection under heavy disease pressure (e.g. in disease nurseries in Lake Bolac, Australia) has been a major achievement in Australian canola breeding and it is the basis of the success of the canola industry to date (Salisbury et al 1995; Raman et al 2020). It could, likewise, be possible to develop FCR tolerant durum varieties by selection under high FCR disease pressure using the methods described in this study.…”

Rotating and stacking genes can improve crop resistance durability while potentially selecting highly virulent pathogen strains

“…Moreover, the reduction in plant genetic and physiological diversity, and the increased homogeneity of modern cropping systems has disrupted selective pressures and the natural co-evolution of plant-pathogen systems 6 , 9 , 10 . Unwanted consequences arise, and the rate at which crop pathogens evolve and overcome host resistance is key 9 , 11 , as the development and deployment of resistant crop varieties is time and resource consuming 12 .…”

Status and advances in mining for blackleg (Leptosphaeria maculans) quantitative resistance (QR) in oilseed rape (Brassica napus)

“…Other than the usual phenotype metrics (plant survival and internal infection), the study also assessed the emerging blackleg symptom of upper canopy infection (UCI) to determine its genetic control. The study found a total of 59 significant SNP associations across 17 chromosomes of B. napus, with most of these SNPs found colocalizing with previous QR-associated genomic regions (Fikere et al 2018(Fikere et al , 2020aFopa Fomeju et al 2014;Jestin et al 2011;Kumar et al 2018;Larkan et al 2016;Rahman et al 2016;Raman et al 2020a). Based on the SNP markers' physical position, chromosomes A04 and A07 were identified as genomic hotspots for blackleg resistance.…”