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ARS Home » Midwest Area » East Lansing, Michigan » Sugarbeet and Bean Research » Research » Publications at this Location » Publication #179787
Title: SUGAR BEET SEEDLING DISEASE RESISTANCE CAUSED BY RHIZOCTONIA

Author
item NAGENDRAN, SUBASHINI - MICHIGAN ST UNIVERSITY
item McGrath, Jon

Submitted to: Annual Beet Sugar Development Foundation Research Report
Publication Type: Research Notes
Publication Acceptance Date: 5/6/2005
Publication Date: 6/1/2005
Citation: Nagendran, S., McGrath, J.M. 2005. Sugar beet seedling disease resistance caused by rhizoctonia. 2004 Annual Beet Sugar Development Foundation Research Report. p. D7-D11.

Interpretive Summary:

Technical Abstract: Early season growth (e.g. the first 10 weeks) is a critical phase of the beet’s life, not only to have good field stands but also to acquire metabolic capacity for agronomic productivity. Early season development includes acquisition of disease tolerance (from acute symptoms with devastating effects to chronic symptoms that only reduce yield potential), and development of the taproot. This change from seedling to adult vegetative growth coincides, in the field, with warming temperatures (and greater seedling disease), increased growth rate, and increased light interception. Rhizoctonia diseases are increasingly important in the Great Lakes growing region, and elsewhere. Genetic resistance is available for the chronic phase of the disease (crown and root rot), and a number of germplasm lines have been released over the past 20 years, which are now becoming available as resistant hybrids available through seed companies. Seedling resistance to Rhizoctonia blight has only recently been reported by this group. The disease progress curves showed three phases of disease reaction on USH20. The initial infection (from zero to 9 days post-inoculation) was characterized by rapid appearance of symptoms, the second phase (from 8 to 13 days of post-inoculation) was characterized by little disease progression, and the final phase (14 to 18 days post-inoculation) finalized the outcome of the interaction, either death (compatible interaction) or recovery (incompatible interaction). cDNA-AFLP was used to follow patterns of gene expression, and experiments are not complete. Preliminary analyses of fragments that were cut from cDNA-AFLP gels, cloned, and sequenced suggested that specific biochemical pathways might be deduced from this approach. Six TDFs from EL51 inoculated with AG2-2 (virulent) and analyzed 4 days after infection could each have a role in limiting spread of Rhizoctonia in the tissue.