Abstract
BackgroundResistance to the blackleg disease of Brassica napus (canola/oilseed rape), caused by the hemibiotrophic fungal pathogen Leptosphaeria maculans, is determined by both race-specific resistance (R) genes and quantitative resistance loci (QTL), or adult-plant resistance (APR). While the introgression of R genes into breeding material is relatively simple, QTL are often detected sporadically, making them harder to capture in breeding programs. For the effective deployment of APR in crop varieties, resistance QTL need to have a reliable influence on phenotype in multiple environments and be well defined genetically to enable marker-assisted selection (MAS).ResultsDoubled-haploid populations produced from the susceptible B. napus variety Topas and APR varieties AG-Castle and AV-Sapphire were analysed for resistance to blackleg in two locations over 3 and 4 years, respectively. Three stable QTL were detected in each population, with two loci appearing to be common to both APR varieties. Physical delineation of three QTL regions was sufficient to identify candidate defense-related genes, including a cluster of cysteine-rich receptor-like kinases contained within a 49 gene QTL interval on chromosome A01. Individual L. maculans isolates were used to define the physical intervals for the race-specific R genes Rlm3 and Rlm4 and to identify QTL common to both field studies and the cotyledon resistance response.ConclusionThrough multi-environment QTL analysis we have identified and delineated four significant and stable QTL suitable for MAS of quantitative blackleg resistance in B. napus, and identified candidate genes which potentially play a role in quantitative defense responses to L. maculans.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-016-0877-2) contains supplementary material, which is available to authorized users.
Highlights
Resistance to the blackleg disease of Brassica napus, caused by the hemibiotrophic fungal pathogen Leptosphaeria maculans, is determined by both race-specific resistance (R) genes and quantitative resistance loci (QTL), or adult-plant resistance (APR)
Host responses to plant pathogens are broadly divided into two categories; basal defense responses induced by generic pathogen signals or elicitors called “pathogen-associated molecular patterns” (PAMPs), resulting in mild defense responses collectively known as ‘Pathogen-associated molecular patterns (PAMP) triggered immunity’ (PTI) and R gene mediated ‘effector triggered immunity’ (ETI) in which race-specific pathogen avirulence (Avr) proteins trigger robust defense mechanisms including hypersensitive response (HR) leading to host cell death at the site of infection [1]
APR is important for combating diseases of Brassica napus L. in which R gene mediated resistance is lacking, such as Sclerotinia Stem Rot (Sclerotinia sclerotiorum) [2,3,4] and Verticillium Wilt (Verticillium longisporum) [5,6,7] or for diseases where pathogen populations often display a rapid adaptation towards R gene mediated resistance, such as in the case of blackleg disease, caused by the hemibiotrophic fungal pathogen Leptosphaeria maculans [8, 9]
Summary
Resistance to the blackleg disease of Brassica napus (canola/oilseed rape), caused by the hemibiotrophic fungal pathogen Leptosphaeria maculans, is determined by both race-specific resistance (R) genes and quantitative resistance loci (QTL), or adult-plant resistance (APR). When studying foliar plant pathogens, the HR response of race-specific R genes often provides a visual phenotype, indicating an incompatible interaction and allowing for the determination of pathogen virulence. This distinction is used to separate specific R gene interactions from quantitative resistance which can provide effective ‘adult plant resistance’ (APR) within a crop variety through the cumulative action of multiple resistance loci. APR is important for combating diseases of Brassica napus L. (canola/oilseed rape) in which R gene mediated resistance is lacking, such as Sclerotinia Stem Rot (Sclerotinia sclerotiorum) [2,3,4] and Verticillium Wilt (Verticillium longisporum) [5,6,7] or for diseases where pathogen populations often display a rapid adaptation towards R gene mediated resistance, such as in the case of blackleg disease, caused by the hemibiotrophic fungal pathogen Leptosphaeria maculans [8, 9]
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