4.5 Article

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

Journal

CROP SCIENCE
Volume 50, Issue 4, Pages 1180-1187

Publisher

CROP SCIENCE SOC AMER
DOI: 10.2135/cropsci2009.10.0589

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Funding

  1. U S Department of Agriculture-Agriculture Research Service [5442-22000-030-00D]
  2. USDA Cooperative State Research, Education, and Extension Service [2005-35301-15728, 2006-55606-16629]
  3. Hatch project [149419]

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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 [Triticum turgidum L. ssp. durum (Desf.) Husn.] background with donor chromosomes originating from three wild emmer [T turgidum L. ssp. dicoccoides (Korn. 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 T dicoccoides 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 I be differentially influenced by the environment. Nonetheless, our results revealed that genes present on five chromosomes, 2A, 2B, 3A, 4A, and 78, 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

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