3 research outputs found

    Mapping and Characterization of Yield Component Traits and Septoria Nodorum Blotch Susceptibility in Wheat

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    Wheat, a major global economic crop and food source, is currently threatened by climate change and the cascading effects, including increased disease pressure. Additionally, wheat yields have not increased significantly for decades, which may impact future food supply. Compared to other crop species, relatively few genes related to wheat yield have been mapped and cloned, with the vast majority in bread, or hexaploid, wheat. In this dissertation, I used three tetraploid wheat populations, Ben × PI 41025 (BP025), Divide × PI 272527 (DP527), and Rusty × PI 193883 (RP883) which were derived from crossing durum cultivars with cultivated emmer accessions. These three populations were evaluated under field conditions in three seasons for 11 traits related to yield. Additionally, the DP527 population was evaluated under greenhouse conditions for these same 11 traits. The known genes ELF3, Ppd-B1, Vrn-A1, Q, Vrn-B1, WAPO-A1, FT-1, GNI-A1, GRF4 and Vrn2 were associated with numerous yield traits. For multiple QTL, the cultivated emmer parent contributed the increased effects. Findings from this study and the identified markers may be useful for breeders who are interested in introgressing the beneficial genes I identified into their germplasm. Here, I also report on the progress and markers developed for fine mapping of a kernels per spike gene that was first mapped in the BP025 population. The work I have done provides a foundation for the cloning of this kernels per spike gene. Lastly, in this dissertation, I screened a global winter wheat panel for genetic regions associated with susceptibility to the necrotrophic pathogen Parastagonospora nodorum, the causal agent of septoria nodorum blotch. I identified the previously cloned genes Tsn1 and Snn3-B1 to be associated with disease caused by the isolates Sn2000 and Sn4, respectively. I also report the first time a panel has been screened for sensitivity to the necrotrophic effectors SnTox267 and SnTox5, along with the prevalence of SnToxA, SnTox1, and SnTox3 sensitivity in this panel. In conclusion, results obtained from these studies provides knowledge of genes/markers which are available to breeders that may provide useful in breeding programs and the overall goal of increasing wheat yield

    Association mapping of resistance to tan spot in the Global Durum Panel

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    Tan spot, caused by the necrotrophic fungal pathogen Pyrenophora tritici-repentis (Ptr), is an important disease of durum and common wheat worldwide. Compared to common wheat, less is known about the genetics and molecular basis of tan spot resistance in durum wheat. We evaluated 510 durum lines from the Global Durum wheat Panel (GDP) for sensitivity to the necrotrophic effectors (NEs) Ptr ToxA and Ptr ToxB, and for reaction to Ptr isolates representing races 1–5. Overall, susceptible durum lines were most prevalent in South Asia, the Middle East, and North Africa. Genome-wide association analysis showed the resistance locus Tsr7 was significantly associated with tan spot caused by races 2 and 3, but not races 1, 4, or 5. The NE sensitivity genes Tsc1 and Tsc2 were associated with susceptibility to Ptr ToxC- and Ptr ToxB-producing isolates, respectively, but Tsn1 was not associated with tan spot caused by Ptr ToxA-producing isolates, which further validates that the Tsn1-Ptr ToxA interaction does not play a significant role in tan spot development in durum. A unique locus on chromosome arm 2AS was associated with tan spot caused by race 4, a race once considered avirulent. A novel trait characterized by expanding chlorosis leading to increased disease severity caused by the Ptr ToxB-producing race 5 isolate DW5 was identified, and this trait was governed by a locus on chromosome 5B. We recommend that durum breeders select resistance alleles at the Tsr7, Tsc1, Tsc2, and the chromosome 2AS loci to obtain broad resistance to tan spot
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