Major Gene and Polygenic Resistance to Leptosphaeria maculans in Oilseed Rape (Brassica napus)

Abstract

The most common and effective way to control phoma stem canker (blackleg) caused by Leptosphaeria maculans in oilseed rape (Brassica napus) is through the breeding of resistant cultivars. Race specific major genes that mediate resistance from the seedling stage have been identified in B. napus or have been introgressed from related species. Many race specific major genes have been described and some of them are probably identical in B. napus (allotetraploid AACC) and the parental species B. rapa (diploid AA). More work is needed using a set of well-characterised isolates to determine the number of different major resistance genes available. In some B. napus cultivars, there is resistance which is polygenic (mediated by Quantitative Trait Loci) and postulated to be race non-specific. Many of these major genes and Quantitative Trait Loci for resistance to L. maculans have been located on B. napus genetic maps. Genes involved in race specific and polygenic resistance are generally distinct.

Molecular mapping of qualitative and quantitative loci for resistance to Leptosphaeria maculans causing blackleg disease in canola (Brassica napus L.)

“…Host resistance genes have been catalogued using differential sets of L. maculans isolates and/or using molecular markers (Delourme et al 2006a;Rouxel et al 2003b). These studies evaluated blackleg resistance on the basis of pathogen infection on cotyledons, stem (canker), and survival under field conditions.…”

“…These studies evaluated blackleg resistance on the basis of pathogen infection on cotyledons, stem (canker), and survival under field conditions. To date, 14 major loci (Rlm1-10 and LepR1 to LepR4) conferring resistance to specific races of L. maculans have been identified (Delourme et al 2006a;Rimmer 2006;Yu et al 2005Yu et al , 2008.…”

“…Previous linkage mapping studies revealed that at least five resistance genes (Rlm1, Rlm3, Rlm4, Rlm 7, and Rlm9) are localised in a cluster within a 40-cM genomic region on chromosome A7 (Delourme et al 2004(Delourme et al , 2006aDion et al 1995;Ferreira et al 1995;Mayerhofer et al 1997;Rimmer 2006;Rimmer et al 1999). This genomic region showed extensive inter-and intra-genomic duplications, as well as intra-chromosomal tandem duplications (Mayerhofer et al 2005).…”

Evolution of virulence in fungal plant pathogens: exploiting fungal genomics to control plant disease

“…For seedling resistance L. maculans has a gene for gene interaction with B. napus. Several resistance genes have been mapped, but only one, LepR3, has been cloned (Delourme et al 2006, van de Wouw et al 2009, Long et al 2011, Larkan et al 2013. Five avirulence genes have been cloned in L. maculans (AvrLm1, AvrLm4-7, AvrLm6, AvrLm11, AvrLmJ1) (Gout et al 2006, Parlange et al 2009, Balesdent et al 2013, van de Wouw et al 2014a).…”

Spatio‐temporal connectivity and host resistance influence evolutionary and epidemiological dynamics of the canola pathogen Leptosphaeria maculans

“…Deployment of new resistance genes to date has been largely ad hoc following discovery and introduction via breeding pathways, resulting in a predictable temporal sequence of pathogen evolutionary adaptation (Van de Wouw et al., 2017). The potential for introduction of new resistances is restricted by a limited germplasm base and the amount of time it takes to develop and evaluate cultivars for commercial use (Delourme et al, 2006). Strategies to maximize the efficacy of R genes in the field are therefore critical for effective and economically viable long‐term disease management as blackleg pressure increases due to rapid expansion and intensification of the canola industry.…”