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A reference-anchored oat linkage map reveals quantitative trait loci conferring adult plant resistance to crown rust (Puccinia coronata f. sp. avenae)

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Abstract

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We mapped three adult plant resistance (APR) loci on oat chromosomes 4D and 6C and developed flanking KASP/PACE markers for marker-assisted selection and gene pyramiding. Using sequence orthology search and the available oat genomic and transcriptomic data, we surveyed these genomic regions for genes that may control disease resistance.

Abstract

Sources of durable disease resistance are needed to minimize yield losses in cultivated oat caused by crown rust (Puccinia coronata f. sp. avenae). In this study, we developed five oat recombinant inbred line mapping populations to identify sources of adult plant resistance from crosses between five APR donors and Otana, a susceptible variety. The preliminary bulk segregant mapping based on allele frequencies showed two regions in linkage group Mrg21 (Chr4D) that are associated with the APR phenotype in all five populations. Six markers from these regions in Chr4D were converted to high-throughput allele specific PCR assays and were used to genotype all individuals in each population. Simple interval mapping showed two peaks in Chr4D, named QPc.APR-4D.1 and QPc.APR-4D.2, which were detected in the OtanaA/CI4706-2 and OtanaA/CI9416-2 and in the Otana/PI189733, OtanaD/PI260616, and OtanaA/CI8000-4 populations, respectively. These results were validated by mapping two entire populations, Otana/PI189733 and OtanaA/CI9416, genotyped using Illumina HiSeq, in which polymorphisms were called against the OT3098 oat reference genome. Composite interval mapping results confirmed the presence of the two quantitative trait loci (QTL) located on oat chromosome 4D and an additional QTL with a smaller effect located on chromosome 6C. This mapping approach also narrowed down the physical intervals to between 5 and 19 Mb, and indicated that QPc.APR-4D.1, QPc.APR-4D.2, and QPc.APR-6C explained 43.4%, 38.5%, and 21.5% of the phenotypic variation, respectively. In a survey of the gene content of each QTL, several clusters of disease resistance genes that may contribute to APR were found. The allele specific PCR markers developed for these QTL regions would be beneficial for marker-assisted breeding, gene pyramiding, and future cloning of resistance genes from oat.

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Data availability

The raw QTL mapping files in qdf format are available at https://github.umn.edu/nazar047/TAG-AdultPlantResistance. Marker information are provided in the supplementary files.

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Acknowledgements

We thank Dr. Marty Carson for identifying the APR donors and developing the mapping populations, and Dr. Shiaoman Chao, Ms. Mary Osenga and Dr. Howard Rines for technical support in genotyping and allele calling. We also acknowledge Mr. Roger Caspers for his valuable help and assistance in the greenhouse and field experiments. This study was funded by USDA-ARS, a graduate student grant from the North Central Region-Sustainable Agriculture, Research, and Education (NCR-SARE) program, MnDRive Global Food Ventures Fellowship, and Doctoral Dissertation Fellowship from the University of Minnesota Graduate School.

Funding

This study was funded by the USDA-ARS. Partial financial support was received from North Central Region-Sustainable Agriculture, Research, and Education (NCR-SARE), MnDRive Global Food Ventures Fellowship, and Doctoral Dissertation Fellowship from the University of Minnesota Graduate School.

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Conceptualization: SK, MF; Methodology: EN, MM, JF; Writing–original draft preparation: Eric Nazareno; Writing–reviewing and editing: all authors; Funding acquisition: SK, MF, EN; Resources: SK, JF; Supervision: SK, MF.

Corresponding author

Correspondence to Shahryar F. Kianian.

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The authors have no conflict of interest to declare.

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Communicated by Xiaoquan Qi.

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Nazareno, E.S., Fiedler, J., Miller, M.E. et al. A reference-anchored oat linkage map reveals quantitative trait loci conferring adult plant resistance to crown rust (Puccinia coronata f. sp. avenae). Theor Appl Genet 135, 3307–3321 (2022). https://doi.org/10.1007/s00122-022-04128-6

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  • DOI: https://doi.org/10.1007/s00122-022-04128-6

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