Mapping and Analysis of Genetic Loci Conferring Resistance to Anthracnose in Lentil

Abstract

Anthracnose, caused by Colletotrichum lentis, is an important fungal disease of lentil in western Canada. Two pathogenic races, race 0 and race 1, have been characterized. Sources of resistance to race 1 are available in the primary gene pool (Lens culinaris), but not for the more virulent race 0. A high level of resistance to race 0 is restricted to Lens ervoides, a wild lentil species in the tertiary gene pool, thus current cultivars of lentil have little or no resistance to race 0. This study comprehensively examined the genetic sources of resistance to race 0 and race 1 in L. culinaris and L. ervoides germplasm. The aims of the thesis project were: 1) to evaluate promising sources of resistance to C. lentis race 0 previously identified in L. culinaris landrace accessions; 2) to identify quantitative trait loci (QTL) conferring resistance to anthracnose race 1 in two lentil biparental recombinant inbred lines (RIL) populations; 3) to perform marker-trait associations for race 1 resistance in lentil via genome-wide association study (GWAS); 4) to identify trait loci associated with both races of anthracnose resistance in L. ervoides accession IG 72815; 5) to create and characterize a BC2-derived lentil advanced backcross (LABC-01) population in cv. CDC Redberry background for L. ervoides genes/alleles derived from the interspecific RIL LR-59-81, and thereby dissect QTL conferring resistance to anthracnose race 0 in the LABC-01 population. The first study evaluated the reaction of 8 promising L. culinaris landrace accessions against race 0 relative to the resistant check LR-59-81. Results revealed lack of effective resistance to race 0 among the accessions tested compared to that of LR-59-81. QTL mapping of the two bi-parental populations identified a major-effect QTL (qAnt1.Lc-3; R2 = 66.6 – 69.8%) that conferred resistance to race 1 on lentil chromosome 3. GWAS detected 14 significant SNPs associated with race 1 resistance on chromosomes 3, 4, 5, and 6. The most significant GWAS SNPs on chromosome 3 colocalized with qAnt1.Lc-3 and delineated a region of 1.6 Mb containing candidate disease resistance genes. A QTL analysis of an interspecific RIL population derived from accession IG 72815 identified major resistance loci on chromosomes 3 and 7 for both races, accounting for 50.2 to 73.3% of the total phenotypic variance. Multiple classes of candidate disease resistance and defense-related genes were uncovered in the intervals of both loci. The LABC-01 population displayed genetic variation for resistance to race 0 and transfer of resistance alleles into the elite cultivar was also evident. A marker-trait association analysis identified a resistance locus (qAnt0.Le-3) on chromosome 3, accounting for 12.5 to 20.7% of the phenotypic variation conferring resistance to race 0. Overall, the research study provides new insights into the inheritance and positions of loci underlying resistance to anthracnose in lentil and lays out an important foundation for marker-assisted introgression of anthracnose resistance from L. ervoides accessions into elite lentil cultivars.