Genetic analysis of kernel texture (grain hardness) in a hard red spring wheat (Triticum aestivum L.) bi-parental population

Authors: BOEHM, JEFFREY - Washington State University; IBBA, MARIA ITRIA - Washington State University; Kiszonas, Alecia; See, Deven; Skinner, Daniel; Morris, Craig

Submitted to: Journal of Cereal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/2/2017
Publication Date: 1/15/2018
Publication URL: https://handle.nal.usda.gov/10113/5844057
Citation: Boehm, J.D., Ibba, M., Kiszonas, A., See, D.R., Skinner, D.Z., Morris, C.F. 2018. Genetic analysis of kernel texture (grain hardness) in a hard red spring wheat (Triticum aestivum L.) bi-parental population. Journal of Cereal Science. 79:57-65.

Interpretive Summary: Wheat kernel texture is a huge determinant of wheat market class both domestically and globally. Wheat is divided into two main classes based upon grain kernel texture: hard or soft. Due to differences in kernel texture, hard and soft wheats mill differently, with varying quantities of break flour yield, total flour yield, starch damage, and flour particle sizes. Compared to soft wheat flours, hard wheat flours have larger particles after mechanical processing and a feature greater amount of damaged starch resulting in higher water absorption when doughs are formed. Hence, hard and soft wheats have different commercial end-uses; hard wheats are used mostly for the production of bread, whereas soft wheats are used mostly for confectionary products. Genetically, kernel texture is controlled by the Hardness (Ha) locus, located on the distal end of chromosome 5DS. Two genes tightly linked to the Ha locus are Puroindoline a (Pin a) and Puroindoline b (Pin b), which express the puroindoline a (PINA) and puroindoline b (PINB) proteins. The presence of these genes and the Ha locus serves to markedly soften wheat kernel texture in hexaploid wheats, with their absence or mutation resulting in the harder kernels of hard winter and spring wheats. In the present study, parent ND2603 carries the Pinb-D1b allele, whereas parent Butte86 carries the Pina-D1b allele, thereby providing an opportunity to identify other sources of genetic variation for kernel texture beyond the two Puroindoline alleles among RILs in the mapping population. Additionally, it was discovered that ND2603 and Butte86 also happen to be polymorphic at the Glu-A1, Glu-B1, Glu-A3, Glu-B3 and Glu-D3 HMW and LMW glutenin loci, thus the RILs are segregating for alleles at these five glutenin loci.

Technical Abstract: Grain hardness is a very important trait in determining wheat market class and also influences milling and baking traits. At the grain Hardness (Ha) locus on chromosome 5DS, there are two primary mutations responsible for conveying a harder kernel texture among U.S. hard red spring wheats: (1) the Pina-D1b or Pina null allele, which lacks the functional expression of the puroindoline a protein, and (2) the Pinb-D1b allele, which features a glycine-to-serine missense mutation in puroindoline b. Herein, hard red spring wheat cultivars Butte86 and ND2603, possessing the Pina-D1b and Pinb-D1b alleles, respectively, were used as parents in the development of 132 recombinant inbred lines (RIL). The RIL population and its parents were phenotyped for single kernel characterization system (SKCS) kernel hardness, NIR hardness, grain protein content, test weight, SK weight, and SK diameter, and genotyped using genotyping-by-sequencing (GBS) technology, SSR markers and allele-specific sequence tagged site markers. Linkage maps for the entire RIL population and for two subsets of RILs, grouped by the inheritance of the Pinb-D1b and Pina-D1b alleles, respectively, were developed using a total of 695 markers in MapDisto version 1.8.1. Multiple QTL mapping identified 29 total QTLs in the population, 6 of which were declared ‘major’ by explaining greater than 15% of the phenotypic variance each for NIR kernel hardness, grain protein content, and test weight. Results also revealed that the high and low molecular weight glutenin loci on chromosome 1B were responsible for kernel hardness variation observed in the mapping population within the Puroindoline allele sub-groups.