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Identification of Chromosome Locations of Genes Affecting Preharvest Sprouting and Seed Dormancy Using Chromosome Substitution Lines in Tetraploid Wheat (Triticum turgidum L.)

Chao, Shiaoman, Xu, Steven S., Elias, Elias M., Faris, Justin D., Sorrells, Mark E.
Crop science 2010 v.50 no.4 pp. 1180
Triticum turgidum subsp. durum, durum wheat, grain crops, Triticum turgidum subsp. dicoccoides, wild relatives, plant genetic resources, genetic variation, chromosome mapping, genes, seed dormancy, grain sprouting, environmental factors, substitution lines, genotype, field experimentation, genetic correlation, phenotypic variation, gene interaction, quantitative trait loci
Seed dormancy, the main factor contributing to preharvest sprouting (PHS) resistance, is a complex trait and is strongly influenced by environmental growth conditions. In this study, three sets of single chromosome substitution lines, including 36 genotypes, in a durum wheat [ L. ssp. (Desf.) Husn.] background with donor chromosomes originating from three wild emmer [ L. ssp. (Körn. ex Asch. and Graebn.) Thell.] accessions were grown in nine field environments and evaluated for seed dormancy and PHS resistance. The substitution lines involving chromosome 3A were among the most dormant genotypes. Germination tests indicated that five chromosomes contained genes influencing seed dormancy at a level comparable to 3A. Results from PHS tests showed that PHS was affected by at least eight chromosomes including 3A. The chromosomes harboring genes for seed dormancy did not fully correspond with those for PHS resistance. The weak correlations between PHS and dormancy observed in this study indicate that different genes are affecting these traits and they may be differentially influenced by the environment. Nonetheless, our results revealed that genes present on five chromosomes, 2A, 2B, 3A, 4A, and 7B, were found to affect both PHS resistance and seed dormancy. These genotypes thus provide useful resources for further studies on genetic interactions that contribute to the overall phenotypic variation and on genetic dissection of quantitative trait loci underlying PHS resistance.