Skip to main content
ARS Home » Midwest Area » Urbana, Illinois » Soybean/maize Germplasm, Pathology, and Genetics Research » Research » Publications at this Location » Publication #321786

Title: Fine mapping of resistance genes from five brown stem rot resistance sources in soybean

Author
item RINCKER, K - University Of Illinois
item Hartman, Glen
item DIERS, BRIAN - University Of Illinois

Submitted to: The Plant Genome
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/17/2015
Publication Date: 2/5/2016
Citation: Rincker, K., Hartman, G.L., Diers, B.W. 2016. Fine mapping of resistance genes from five brown stem rot resistance sources in soybean. The Plant Genome. doi:10.3835/plantgenome2015.08.0063.

Interpretive Summary: Brown stem rot (BSR) of soybean is caused by a soil fungal pathogen. Soybean production in the northern U.S., Canada, and Brazil has been compromised with yield losses of up to 38% reported from BSR. Management of this disease can be achieved with host genetic resistance. Three BSR resistance genes (Rbs1, Rbs2, and Rbs3) have been previously identified and mapped to a single region on chromosome 16. The objective of this study was to fine map the positions of these resistance genes from five sources. BSR resistance was mapped to intervals ranging from 0.34 to 0.04 Mb in the different sources, which provided further evidence that only one locus provides BSR resistance in soybean. These results will aid future research on marker-assisted selection and gene cloning by providing a narrowed genomic interval containing an Rbs gene. This research is important to scientists interested in host resistance genes for managing soybean diseases.

Technical Abstract: Brown stem rot (BSR) of soybean [Glycine max (L.) Merr.] caused by Cadophora gregata (Allington & Chamb.) T.C. Harr. & McNew, can be controlled effectively with genetic host resistance. Three BSR resistance genes Rbs1, Rbs2, and Rbs3, have been identified and mapped to a large region on chromosome 16. Marker-assisted selection will be more efficient and gene cloning will be facilitated with a narrowed genomic interval containing an Rbs gene. The objective of this study was to fine map the positions of Rbs genes from five sources. Mapping populations were developed by crossing the resistant sources ‘Bell’, PI 84946-2, PI 437833, PI 437970, L84-5873, and PI 86150 with either the susceptible cultivar Colfax or Century 84. Plants identified as having a recombination event near Rbs genes were selected and individually harvested to create recombinant lines. Progeny from recombinant lines were tested in a C. gregata root-dip assay and evaluated for foliar and stem BSR symptom development. Overall, 4,878 plants were screened for recombination and progeny from 52 recombinant plants were evaluated with simple sequence repeat genetic markers and assessed for symptom development. BSR resistance was mapped to intervals ranging from 0.34 to 0.04 Mb in the different sources. In all sources, resistance was fine mapped to intervals inclusive of BARCSOYSSR_16_1114 and BARCSOYSSR_16_1115, which provides further evidence that one locus provides BSR resistance in soybean.