Identification of markers linked to genes for sprouting tolerance (independent of grain color) in hard white winter wheat (HWWW)

Authors

Juthamas Fakthongphan, University of Nebraska-Lincoln
Guihua Bai, USDA-ARSFollow
Paul St. Amand, USDA-ARSFollow
Robert A. Graybosch, USDA-ARSFollow
P. Stephen Baenziger, University of Nebraska-LincolnFollow

ORCID IDs

P. Stephen Baenziger

Document Type

Article

Date of this Version

2016

Citation

Theor Appl Genet (2016) 129:419–430, DOI 10.1007/s00122-015-2636-4.

Comments

U.S. government work.

Abstract

Key message Hard red wheats can donate genes to hard white wheats for tolerance to preharvest sprouting, the effects are quantitative in nature, and may be tracked with previously described DNA markers.

Abstract Pre-harvest sprouting (PHS) of wheat (Triticum aestivum L.) can negatively impact end-use quality and seed viability at planting. Due to preferences for white over red wheat in international markets, white wheat with PHS tolerance has become increasingly desired for worldwide wheat production. In general, however, red wheat is more tolerant of sprouting than white wheat. The main objective of this study was the identification of PHS tolerance conditioned by genes donated from hard red winter wheat, using markers applicable to the Great Plains hard white wheat gene pool. Three red wheat by white wheat populations, Niobrara/NW99L7068, NE98466/NW99L7068 and Jagalene/ NW99L7068 were developed, and white-seeded progenies were analyzed for PHS tolerance and used to identify markers for the trait. In the three populations, marker loci with significant allelic effects were most commonly located on chromosomes of group 2, 3, 4 and 5, though additional markers were detected across the wheat genome. Chromosome 3A was the only chromosome with significant markers in all three populations. Markers were inconsistent across the three populations, and markers linked to tolerance-inducing loci were identified in both tolerant and susceptible parents. Additive effects of marker loci were common. In the present investigation, a wide range of PHS tolerance was observed, even though all lines were fixed for the recently reported positive TaPHS1 allele. PHS tolerance is controlled by additive major gene effects with minor gene effects where variations of minor gene effects were still unclear.