Quantitative resistance (QR) to blackleg crown canker, caused by the fungal pathogen Leptosphaeria maculans, is an important component of disease management in canola. QR is a complex trait whose underlying genetics remain poorly understood. Reliable phenotyping methods for QR are critical for accurate assessment and breeding. However, the relative contributions of host genetics, pathogen genetics, and environmental factors to phenotypic variation and stability are not well understood or quantified. Developing a better understanding of these complexities is crucial for advancing resistance breeding and phenotyping strategies.
This study aimed to dissect the drivers of phenotypic variation in quantitative resistance to blackleg, with a focus on the relative contributions of host and pathogen genetics, and environment. It further investigated the complex, plastic nature of quantitative resistance, and explanations for phenotypic variance independent of genetic and environmental components. Using a hybrid field-glasshouse approach, three canola cultivars with differing resistance profiles were inoculated with three controlled pathogen sources across three environments: Horsham, Wagga Wagga, and Boorowa. Plants were grown to maturity and at harvest, a total of 6,825 replicate plants were scored for crown canker severity. Mixed-effects models were applied to quantify the contributions of main effects and interactions, including three-way interactions, to phenotypic variation. Significant variation was observed in resistance expression, strongly influenced by environmental conditions and canola cultivar. Evidence of pathogen-specific responses was detected, suggesting a complex interplay between host genotype and pathogen identity. Notably, three-way interactions among cultivar, environment, and pathogen source explained a substantial portion of the phenotypic variation, though a significant proportion of variance remained unexplained.
This study highlights the complex nature of quantitative resistance, the expression of which is shaped by phenotypic plasticity, environmental variation and pathogen genetics. High levels of unexplained variance have potential to complicate future genetic studies and will require further development and refinement of high-throughput, field-based phenotyping methods.