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ARS Home » Pacific West Area » Salinas, California » Crop Improvement and Protection Research » Research » Publications at this Location » Publication #205939
Title: Rhizomania as seen from inside the beet cell: Identifying proteome differences between sugarbeet infected with Beet necrotic yellow vein virus and healthy sugarbeet

Author
item Larson, Rebecca
item Nunez, Angelika
item Wintermantel, William - Bill

Submitted to: Plant and Animal Genome
Publication Type: Abstract Only
Publication Acceptance Date: 9/28/2006
Publication Date: N/A
Citation: N/A

Interpretive Summary: Rhizomania, caused by Beet necrotic yellow vein virus (BNYVV) is one of the most economically important diseases affecting sugarbeet. The disease is characterized by excessive growth of lateral roots and constriction of the taproot, the main sucrose storage site in sugarbeet, resulting in decreased sugar yield. The importance of this disease has been reemphasized by the emergence of new resistance breaking isolates in many areas where resistant sugarbeet is universally planted. This project focuses on identification of proteins induced or repressed during BNYVV infection, with a goal of determining key protein interactions between BNYVV and sugarbeet that contribute to disease. Closely related sugarbeet lines varying for the presence/absence of the Rz1 resistance allele were grown under identical environmental conditions in a growth chamber in noninfested soil or soil infested with BNYVV. At three and six weeks after planting, plant material was tested to confirm the presence/absence of BNYVV, and total plant protein was extracted from roots, quantified and fractionated using multidimensional liquid chromatography. Subtractive proteomics determined that only approximately 20 percent of the sugarbeet proteome was influenced during BNYVV infection compared with healthy sugarbeet. Protein identification using tandem MALDI-TOF-MS and sequence analysis has identified several major proteins influenced by infection that are known to be involved in cellular defense, including polyphenol oxidase, germin-like proteins, polyubiquitin and chitinase among others. Downstream analysis will involve arrays for the identification of interactions between BNYVV and sugarbeet proteins in an effort to identify key interactions driving infection and symptom development.

Technical Abstract: Rhizomania, caused by Beet necrotic yellow vein virus (BNYVV) is one of the most economically important diseases affecting sugarbeet. The disease is characterized by excessive growth of lateral roots and constriction of the taproot, the main sucrose storage site in sugarbeet, resulting in decreased sugar yield. The importance of this disease has been reemphasized by the emergence of new resistance breaking isolates in many areas where resistant sugarbeet is universally planted. This project focuses on identification of proteins induced or repressed during BNYVV infection, with a goal of determining key protein interactions between BNYVV and sugarbeet that contribute to disease. Near isogenic sugarbeet lines varying for the presence/absence of the Rz1 resistance allele were grown under identical environmental conditions in a growth chamber in noninfested soil or soil infested with BNYVV. At three and six weeks after planting, plant material was tested to confirm the presence/absence of BNYVV, and total plant protein was extracted from roots, quantified and fractionated using multidimensional liquid chromatography. Subtractive proteomics determined that only approximately 20 percent of the sugarbeet proteome was influenced during BNYVV infection compared with healthy sugarbeet. Protein identification using tandem MALDI-TOF-MS and sequence analysis has identified several major proteins influenced by infection that are known to be involved in cellular defense, including polyphenol oxidase, germin-like proteins, polyubiquitin and chitinase among others. Downstream analysis will involve arrays for the identification of interactions between BNYVV and sugarbeet proteins in an effort to identify key interactions driving infection and symptom development.