Submitted to: Plant Disease Management Reports
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 16, 2013
Publication Date: August 14, 2013
Citation: Panella, L.W., Strausbaugh, C.A. 2013. Beet curly top resistance in USDA-ARS Plant Introductions, 2012. Plant Disease Management Reports. 7:FC121. Interpretive Summary: Rhizomania is a disease of sugar beet, caused by Beet Necrotic Yellow Vein Virus (BNYVV) which severely impacts sugarbeet in all production regions. Little is known about how the plant responds to infection with BNYVV nor the mechanisms of resistance. Proteomic profiling was conducted on susceptible sugar beet infected with BNYVV to identify proteins that are expressed during susceptible virus-plant interactions. A total of 215 proteins were identified, with a predominance of proteins associated with photosynthesis and energy, metabolism, and plant defense. Many of the identified proteins have been previously associated with systemic acquired resistance and general plant defense responses particularly those mediated by reactive oxygen species. These results expand on limited proteomic data available for sugarbeet and provide the ground work for future studies focused on understanding the interaction of BNYVV with sugarbeet.
Technical Abstract: Thirty sea beet (Beta vulgaris subsp. maritima (L.) Arcang) and beet (Beta vulgaris subsp. vulgaris L.) plant introduction (PI) accessions from the Beta collection of the USDA-ARS National Plant Germplasm System were screened for resistance to Beet severe curly top virus (BSCTV) and other closely related Curtovirus species in 2012. Commercial cultivars Monohikari and HM PM90 and Betaseed, Inc. germplasm line G6040 were included as susceptible and resistant checks. The curly top evaluation was conducted at the USDA-ARS North Farm in Kimberly, ID which has Portneuf silt loam soil and had been in alfalfa in 2011. The field was plowed in the fall and in the spring, fertilized (90 lb N and 110 lb P2O5/A) on 16 Apr 12, sprayed with Ethotron (2 pt/A), and roller harrowed. The germplasm was planted (density of 142,560 seeds/A) on 21 May. The plots were two rows 10 ft long with 22-in row spacing and arranged in a randomized complete block design with three replications. The fields were sprinkler irrigated and hand weeded as necessary. Plant populations were thinned to about 47,500 plants/A on 19 Jun. Plants were inoculated at the four to six leaf growth stage on 22 Jun with six viruliferous beet leafhoppers per plant. The beet leafhoppers were moved twice a day (right after sunrise and just before sunset) for one week by dragging a tarp through the field. The plants were sprayed with Lorsban 4E (1.5 pints/A) on 4 Jul to kill the beet leafhoppers. The plots were rated for foliar symptom development on 10 Jul using a scale of 0-9 (0 = healthy and 9 = dead; Mumford 1974), with disease index (DI) treated as a continuous variable. Data were analyzed using the general linear models procedure (Proc GLM-SAS), and Fisher’s protected least significant difference was used for mean comparisons. Disease development was uniform and other disease problems were not evident in the plot area. The disease pressure in the test was severe with good disease development in the more susceptible lines. Most of the lines were not significantly different from the most resistant check. These accessions will be retested and, if the resistance is confirmed, entered into USDA-ARS breeding programs to enhance sugar beet germplasm with increased resistance to Beet severe curly top virus (BSCTV) and other closely related Curtovirus species. These data will be entered into the USDA-ARS, NPGS GRIN database (http://www.ars-grin.gov/npgs/index.html).