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United States Department of Agriculture

Agricultural Research Service

Research Project: NONCHEMICAL PEST CONTROL AND ENHANCED SUGAR BEET GERMPLASM VIA TRADITIONAL AND MOLECULAR TECHNOLOGIES

Location: Sugarbeet Research

2008 Annual Report


1a.Objectives (from AD-416)
Objective 1: Evaluate, characterize, and utilize available sugarbeet genetic resources and ascertain the diversity (genetic, proteomic, morphological, and pathogenic) within and among sugarbeet and sugarbeet pathogen populations to fulfill the objectives below. This objective is an important part of the ARS NPGS Beta germplasm collection, which is available to public and private breeders and geneticists. Sub-objective 1a: Determine the spatial scale of genetic differentiation among populations of B. nana.

Objective 2: Characterize the interaction of major sugarbeet pathogens (esp. Beet necrotic yellow vein virus, Cercospora beticola, Rhizoctonia solani, and Fusarium oxysporum) with sugarbeet. Sub-Objective 2a: Apply proteomics protocols to understand Beet necrotic yellow vein virus-sugar beet interactions. Sub-Objective 2b: Using comparative proteomics, determine the degree of conservation of defense response against a variety of Fusarium spp. Sub-Objective 2c: Determine role of ubiquitination and the proteosome pathway in activation of plant defense.

Objective 3: Develop and distribute enhanced germplasm with novel stress resistance genes.


1b.Approach (from AD-416)
Objective 1 A multidisciplinary approach combining traditional genetics, molecular biology, and biochemistry will characterize variation among sugarbeet wild relatives and cultivated beets. Understanding the diversity within the NPGS Beta PI collection is necessary to both intelligently manage and utilize the germplasm stored in this collection. Understanding of the diversity contained in our commercial lines is necessary to most effectively introduce new diversity into them. Understanding the genetic variability of pathogen populations is extremely important to maintaining durable host plant resistance. The same classical and molecular tools will be used to gain the knowledge of genetic diversity in the pathogens, which is critical for selecting the number and pathotype of organisms to use in resistance screening. Objective 2 This multidisciplinary approach combining traditional genetics, molecular biology, and biochemistry will be used for identification of key genes or proteins involved in the sugar beet pathogen interaction. Characterization using varied techniques provides a better understanding of plant defense against disease and identifies candidate genes and novel sources of resistance to move into sugar beet germplasm. Furthermore, this greater knowledge of sugar beet pathogen interaction opens up avenues for creating novel selection tools, including exploitation of polymorphisms and use of biomarkers. The same analyses can be used to understand and better manage pathogens of sugar beet, creating novel, more effective disease control strategies. Objective 3 The basis of the breeding program is the formation of long range breeding populations through the introgression of resistant germplasm from “exotic” sources of the primary Beta germplasm pool (Beta vulgaris ssp. maritima, fodder beet, table beet, Swiss chard, foreign sugar beet landraces from the PI collection, etc.). This breeding scheme provides great flexibility to accommodate the genetic background of the germplasm and the disease resistances being chosen. The development of breeding populations will be accomplished using methods that produce genetically defined sub populations, which are useful for resistance gene mapping, marker development, exploring sugarbeet-pathogen interactions, and gene discovery.


3.Progress Report
This is the initial report for Project 5402-21220-007-00D, which began its 5 year duration March 11, 2008. Some of this research is continued from Project 5402-21220-006-00D

Progress was made in breeding populations with resistance to sugarbeet cyst nematode, cercospora leaf spot, fusarium yellows, and rhizoctonia root rot. Breeding and disease evaluation nurseries were planted and inoculated. The inoculated nurseries were to screen for resistance to rhizoctonia root rot and fusarium yellows. Resistant germplasms FC220 and FC221 were registered in the Journal of Plant Registrations.

Fusarium yellows, caused by the fungus Fusarium oxysporum f. sp. betae (FOB), can lead to significant yield losses for sugar beet growers. This fungus is variable in pathogenicity, morphology, host range, and symptoms; and, it is not a well characterized pathogen on sugar beet. A phylogenetic study of the genetic variability among isolates of fusarium oxysporum from sugar beet based upon sequence data from ß- tubulin, EF1a, and ITS was submitted for publication.

Rhizomania, caused by Beet necrotic yellow vein virus, is a serious threat to sugar beet production worldwide. The main symptom of this disease is massive overgrowth of lateral roots, called hairy root. A manuscript examining proteome changes in sugar beet in response to Beet necrotic yellow vein virus was accepted and published.

This addresses NP301 Action Plan objective 3C, Germplasm Enhancement/Release of Improved Genetic Resources and Varieties.


4.Accomplishments
1. Problem: Much of the disease resistant germplasm released by the USDA-ARS breeding programs do not contain resistance to rhizomania. Rhizomania, caused by Beet necrotic yellow vein virus, is a serious threat to sugar beet production worldwide, and resistant germplasm is the primary means of managing this disease. Accomplishment: Two sugar beet multigerm germplasms, ‘FC220 and ‘FC221”, were released and registered. These germplasms combine between them resistances to rhizoctonia root rot (AG-2-2), rhizomania, aphanomyces root rot (aphanomyces black root), curly top, sugarbeet root aphid, and cercospora leaf spot. They have favorable yield characteristics when evaluated as lines or in experimental hybrids under rhizomania conditions at Salinas, CA. Impact: These germplasms have been released to public and private plant breeders and plant scientists world-wide. They offer resistances to important sugar beet diseases in a rhizomania resistant genetic background.

This addresses NP301 Action Plan objective 3C, Germplasm Enhancement/Release of Improved Genetic Resources and Varieties.


5.Significant Activities that Support Special Target Populations
None.


6.Technology Transfer

None

Review Publications
Larson, R.L., Wintermantel, W.M., Hill, A.L., Fortis, L.L., Nunez, A. 2008. Proteome changes in sugar beet in response to Beet necrotic yellow vein virus. Physiological and Molecular Plant Pathology. doi:10.1016/j.pmpp.2008.04.003

Panella, L.W., Fenwick, A.L., Hill, A.L., Mcclintock, M.E., Vagher, T.O. 2008. Rhizoctonia root rot resistance of Beta PIs from the USDA-ARS NPGS, 2007. Plant Disease Management Reports. (online) 2:V057.DOI:10.1094/PDMR02. The American Phytopathological Society. St. Paul, MN.

Panella, L.W., Hanson, L.E., Lewellen, R.T. 2008. Breeding for Multiple Disease Resistance in Sugarbeet: Registration of FC220 and FC221. Journal of Plant Registrations.

Hanson, L.E., Panella, L.W. 2007. Rhizoctonia root rot resistance of Beta PIs from the USDA-ARS NPGS, 2006. Plant Disease Management Reports. (online) 1:V023. DOI: 10.1094/PDMR01. The American Phytopathological Society. St. Paul, MN.

Larson, R.L., Hill, A.L., Nunez, A. 2007. Characterization of Protein Changes Associated with Sugar Beet (Beta vulgaris) Resistance and Susceptibility to Fusarium oxysporum.. Journal of Agricultural and Food Chemistry. 55:7905-7915.

Last Modified: 4/16/2014
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