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ARS Home » Midwest Area » East Lansing, Michigan » Sugarbeet and Bean Research » Research » Publications at this Location » Publication #219653
Title: Identification of Sugar Beet Germplasm EL51 as a Source of Resistance to Post-Emergence Rhizoctonia Damping-Off

Author
item NAGENDRAN, SUBASHINI - MICHIGAN STATE UNIVERSITY
item HAMMERSCHMIDT, RAY - MICHIGAN STATE UNIVERSITY
item McGrath, Jon

Submitted to: European Journal of Plant Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/2/2008
Publication Date: 2/1/2009
Citation: Nagendran, S., Hammerschmidt, R., McGrath, J.M. 2009. Identification of Sugar Beet Germplasm EL51 as a Source of Resistance to Post-Emergence Rhizoctonia Damping-Off. European Journal of Plant Pathology. 123:461-471.

Interpretive Summary: Seedling diseases seriously affect sugar beet production by killing young plants and reducing the number of plants that would have been harvested otherwise. Among the more serious seedling diseases of sugar beet in Michigan are those caused by the fungus Rhizoctonia. The infection process that leads to damping-off and seedling death was characterized in two-week-old sugar beet seedlings in growth chamber, greenhouse, and field nurseries. Results indicated a predictable disease progress pattern that leads to either a diseased or non-diseased state depending on the virulence of the fungus. Germplasm was screened to see if there is any Rhizoctonia damping-off resistance in the cultivated beets. One previously released ARS sugar beet, EL51, showed a high level of resistance to the most virulent isolate of Rhizoctonia tested. Identification of resistance to Rhizoctonia damping-off is a major accomplishment that will allow commercial deployment of this trait, potentially saving growers millions of dollars, and allow scientists to better understand host-pathogen interactions in this very destructive disease.

Technical Abstract: The basidiomycete Rhizoctonia solani is a major agent of seedling stand declines in Michigan sugar beet production. Disease progress, starting from 2-week-old sugar beet seedlings, was scored daily over the following ca. two weeks in a controlled environment, using two AG-2-2 isolates and two AG-4 isolates, each AG group represented by a high- and low-virulence isolate. All isolates infected seedlings as evidenced by an infection scar at the base of the hypocotyl, however only AG-2-2 isolate R-1 caused seedling death in a susceptible hybrid. The two AG-4 isolates and the AG-2-2 isolate W22 showed a characteristic pattern of disease progression in the growth chamber where disease index (DI) values increased for the first 5-6 days, were relatively constant for the next 7-8 days, and declined thereafter. AG-2-2 R-1 inoculated plants under the same conditions showed similar patterns for the first 4 days post-inoculation, however DI’s continued increasing until seedling death at 13-14 days. This screen was applied to a range of germplasm, and one line, EL51, previously field-selected for resistance to crown and root rot, survived seedling inoculation with AG-2-2 R-1. In a field disease nursery artificially inoculated with AG-2-2 R-1 at the seedling stage, seedling persistence was high with EL51, but not with a susceptible hybrid. Identification of EL51 as a source of resistance to Rhizoctonia damping-off may allow deeper basic investigations into the Beta-Rhizoctonia pathosystem, as well as be valuable for sugar beet breeding.