Abstract

Kernel color and grain protein concentration (GPC) are two of the most important attributes of barley (Hordeum vulgare L.) grain intended for use in malting and brewing. Grain with protein levels that are too low or high or that have dark kernel color, which may result from the disease complex of kernel discoloration (KD), is unacceptable for the malting and brewing industries. The purpose of this study was to use molecular markers to map quantitative trait loci (QTLs) for KD and GPC in two recombinant inbred line (RIL) populations. One population was created by means of the high GPC and KD resistant cultivar Chevron. The other population was created from a KD resistant cultivar MNBrite that was derived from Chevron through eight generations of crossing and selection for bright kernels. The traits KD and GPC were evaluated in four and three environments, respectively, using the Chevron population and six environments using the MNBrite population. GPC and KD score were negatively correlated in both populations. A revised genetic map for the Chevron/M69 population, with an additional 45 simple sequence repeat (SSR) markers, was used to identify nine QTLs associated with KD on chromosomes 1(7H), 2(2H), 4(4H), 6(6H), and 7(5H), including two major QTLs on chromosome 6(6H). A single QTL for GPC identified in the Chevron mapping population, accounting for over 55% of the phenotypic variation, was located on chromosome 6(6H) and was coincident with one of the two major QTLs for KD. In this region, the Chevron allele increased GPC and decreased KD score. In the MNBrite mapping population, the same region of chromosome 6(6H) was mapped with SSR markers, and QTL analysis verified that this region was associated with both KD and GPC, indicating that MNBrite inherited this region of chromosome 6(6H) from Chevron. The results of this study suggest that if GPC and KD are controlled by tightly linked genes, then it should be possible to use SSR markers to identify recombinants in this region of chromosome 6(6H) and break the linkage to allow selection for KD resistance without high GPC. Alternatively, if GPC and KD are conditioned by the same gene, then it should be possible to select for KD resistance from Chevron by means of SSR markers and to use phenotypic selection to introgress other genes to reduce GPC to acceptable levels.

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