Background

Fusarium head blight (FHB) is currently the most important disease of barley in the midwestern United States. The major loss is due to contamination of harvested grain with deoxynivalenol (DON) that results in downgrading of grain from malting to feed quality. The variety 'Chevron' shows resistance to FHB, the resistance being evident in the low DON levels in grain. Chevron is also a source of resistance to kernel discoloration (KD). The objectives of this study were to understand the genetic basis of resistance to FHB and KD in Chevron; and to identify molecular markers for marker-assisted selection of FHB and KD resistant genotypes.

Genetics of resistance

Segregation for reactions to FHB and KD, and to DON concentration were determined using the Chevron/M69 recombinant inbred line population. Results indicated that these traits were quantitatively inherited and the distributions extended beyond the parents. Resistance to FHB and KD, and low DON levels were positively correlated to each other, and were negatively correlated with heading date and plant height. These results indicate that selection for low KD score, which is relatively easy to evaluate, could lead to resistance to FHB and low DON level. However, negative correlations between resistance to these diseases and to late heading and tallness may indicate pleiotrophic effects.

Genetic mapping

QTLs associated with resistances to FHB and KD, and to low DON concentration, were mapped based on RFLPs. The Chevron/M69 RFLP linkage map currently has 93 marker loci and 18 linkage groups. Markers on linkage groups located on chromosomes 1, 2, 5, and 6 detected QTLs conferring resistances to FHB and KD, and to low DON concentration. The QTL conferring resistance to FHB on chromosome 5 came from M69. Markers on chromosomes 1 and 2 also were associated with late heading and tallness. Linked markers explained 40, 50, and 45% of variation among lines for resistance to FHB and KD, and to reduced DON production, respectively. Positive correlations and similar chromosomal locations between FHB and KD suggest that resistance to these diseases may be conferred by the same or closely-linked genes. Additional markers are currently being screened to saturate chromosomal regions containing genes for resistance to FHB and KD, and to increase coverage of the linkage map.