Poster
Alyssa Flobinus
Department of Plant Pathology, North Dakota State University
Fargo, North Dakota, United States
John J. Weiland
USDA- ARS retired employee
Fargo, North Dakota, United States
Carla M. R. Varanda
Research Centre for Natural Resources, Environment and Society (CERNAS), Santarém Polytechnic University, Santarém Agrarian School
Santarem, Santarem, Portugal
Patrick Materatski
MED—Mediterranean Institute for Agriculture, Environment and Development & CHANGE—Global Change and Sustainability Institute, Institute for Advanced Studies and Research, Universidade de Évora
Evora, Evora, Portugal
Zachary Ittel
Department of Plant Pathology, North Dakota State University
Fargo, North Dakota, United States
Karen Fugate
USDA-ARS Edward T. Schafer Agricultural Research Center
Fargo, North Dakota, United States
John Eide
USDA-ARS Edward T. Schafer Agricultural Research Center
Fargo, North Dakota, United States
Gary A. Secor
Department of Plant Pathology, North Dakota State University
Fargo, North Dakota, United States
Melvin D. Bolton
USDA-ARS Edward T. Schafer Agricultural Research Center
Fargo, North Dakota, United States
Sugarbeet (Beta vulgaris L.) is a major crop providing approximately 20% of global sucrose. Viral diseases affecting sugarbeet impact sugar yield and lead to significant financial losses for growers. Recently, our laboratory identified a new Alphanecrovirus nicotianae variant named Beta vulgaris Alphanecrovirus-1 (BvANV-1) in rhizomania-diseased sugarbeet roots. Alphanecrovirus nicotianae infects a wide host range, inducing necrotic symptoms on inoculated leaves and/or systemic infection in some hosts. The host range of BvANV-1 was determined using two DNA-based clones, BvANV-1 wild type and clone #7, the latter of which carried three mutations; one non-synonymous mutation in the replicase gene (p23), one synonymous mutation in p23, and one synonymous mutation in the movement protein gene (p8). Viral transmission by Olpidium virulentus was verified in sugarbeet using both clones. Our study revealed variation in virulence between clones on selected hosts, highlighting the importance of the mutations found in clone #7. Using site-directed mutagenesis of clone #7, we demonstrated that the amino acid change in p23 gene alone restored the wild type phenotype on inoculated leaves. Moreover, the addition of the synonymous mutation in p8 was required to establish a systemic infection in N. benthamiana similar to wild type. Taken together, our analyses characterized the role of p23 and p8 during BvANV-1 infection and a potential new viral pathogen of sugarbeet and rotational crops.