Author
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Wintermantel, William - Bill |
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Gulati Sakhuja, Anju |
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LARSON, R - Syngenta |
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Hladky, Laura |
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Nunez, Alberto |
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Hill, Amy |
Submitted to: American Society of Sugar Beet Technologists
Publication Type: Proceedings Publication Acceptance Date: 6/30/2009 Publication Date: 6/30/2009 Citation: Wintermantel, W.M., Gulati Sakhuja, A.N., Larson, R.L., Hladky, L.L., Nunez, A., Hill, A.L. 2009. Proteome changes in sugarbeet in response to Beet necrotic yellow vein virus infection.Proc. Of the 35th biennial meeting of the American Society of Sugar Beet Technologists, Feb. 25-28, 2009, Orlando, FL: “Growing and Breeding,” Sections B&E Physiology, Biotechnology, Genetics and Germplasm. (Published CD) Interpretive Summary: Rhizomania, caused by Beet necrotic yellow vein virus (BNYVV), is characterized by excessive growth of lateral roots and constriction of the taproot, resulting in decreased sugar yield. There are limited sources of resistance against the virus and resistance-breaking isolates are becoming increasingly problematic worldwide. Developing more effective disease control strategies starts with gaining a better understanding of the basis for resistance and the mechanism of disease. Multidimensional liquid chromatography was employed to examine proteins differentially expressed in nearly isogenic lines of sugar beet either resistant or susceptible to BNYVV infection. More than 1,000 protein peaks were reproducibly detected in the root extracts from each treatment. Differential protein expression in response to viral inoculation was determined by comparing healthy and BNYVV-challenged chromatogram protein profiles for each sugarbeet genotype. Protein expression was temporally regulated, and in total, 7.4 and 11% of the detected proteome was affected by BNYVV-challenge in the resistant and susceptible genotypes, respectively. Sixty-five of the proteins induced or repressed by the virus were identified by tandem MALDI-TOF mass spectrometry and expression of key defense- and disease-related proteins was further verified using qualitative reverse transcriptase polymerase chain reaction. Results suggest involvement of classic systemic resistance components in Rz1-mediated resistance and phytohormones in hairy root symptom development. Follow-up studies seek to identify key virus-sugarbeet protein interactions driving infection and symptom development, and to utilize this information to develop novel methods for rhizomania resistance. Technical Abstract: Rhizomania, caused by Beet necrotic yellow vein virus (BNYVV), is characterized by excessive growth of lateral roots and constriction of the taproot, resulting in decreased sugar yield. There are limited sources of resistance against the virus and resistance-breaking isolates are becoming increasingly problematic worldwide. Developing more effective disease control strategies starts with gaining a better understanding of the basis for resistance and the mechanism of disease. Multidimensional liquid chromatography was employed to examine proteins differentially expressed in nearly isogenic lines of sugar beet either resistant or susceptible to BNYVV infection. More than 1,000 protein peaks were reproducibly detected in the root extracts from each treatment. Differential protein expression in response to viral inoculation was determined by comparing healthy and BNYVV-challenged chromatogram protein profiles for each sugarbeet genotype. Protein expression was temporally regulated, and in total, 7.4 and 11% of the detected proteome was affected by BNYVV-challenge in the resistant and susceptible genotypes, respectively. Sixty-five of the proteins induced or repressed by the virus were identified by tandem MALDI-TOF mass spectrometry and expression of key defense- and disease-related proteins was further verified using qualitative reverse transcriptase polymerase chain reaction. Results suggest involvement of classic systemic resistance components in Rz1-mediated resistance and phytohormones in hairy root symptom development. Follow-up studies seek to identify key virus-sugarbeet protein interactions driving infection and symptom development, and to utilize this information to develop novel methods for rhizomania resistance. |