Location: Sugarbeet and Potato ResearchTitle: Analysis of the P25 Pathogenicity Factor of Beet necrotic yellow vein virus strains from North Dakota and Minnesota Author
|Bornemann, Kathrin - North Dakota State University|
|Khan, Mohamed - North Dakota State University|
Submitted to: Plant Disease
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/2/2019
Publication Date: N/A
Interpretive Summary: Rhizomania is a disease of sugarbeet found throughout the world. The disease is caused by Beet necrotic yellow vein virus. Until recently, the disease has been kept in check by farmers planting sugarbeet varieties with the Rz1 resistance gene. However, 'resistance-breaking' strains of the virus have emerged that can still cause disease on varieties harboring Rz1. Past research has suggested there is a strong correlation between the ability of the virus to break Rz1-encoded resistance and mutations in the viral P25 gene. In this study, we obtained nearly 600 soil samples from the Red River Valley of MN and ND and attempted to "bait" the virus from the soil using susceptible sugarbeet varieties and those with Rz1 and other resistance genes. Unexpectedly, we could not find a strong association between mutations in P25 and the ability to break resistance of any resistance gene. These results shed new light on rhizomania disease physiology and put new importance on the development of lines with resistance to this disease of global importance.
Technical Abstract: Beet necrotic yellow vein virus (BNYVV) is the causal agent of rhizomania, a disease of global importance to the sugar beet industry. The most widely implemented resistance gene to date is Rz1, but resistance has been circumvented by resistance-breaking (RB) isolates world-wide. The BNYVV P25 gene encodes a recognized pathogenicity and virulence factor and specific alleles of this gene have been found to be associated with the RB type. In an effort to gain greater understanding of the distribution of BNYVV and the nature of RB in Minnesota and eastern North Dakota, 594 soil samples obtained from sugar beet production fields were analyzed for the presence of BNYVV as well as coding variability in the P25 gene. Baiting of virus from the soil with sugar beet varieties possessing no known resistance to rhizomania resulted in a disease incidence level of 10.6% in the region examined. Parallel baiting analysis of sugar beet genotypes possessing Rz1, the more recently introgressed Rz2, and with the combination of Rz1+Rz2, resulted in the recovery of P25 gene-specific amplicons in all treatment categories tested. Virus sequences recovered from sugar beet bait plants possessing resistance genes Rz1 and/or Rz2 exhibited reduced genetic diversity in the P25 gene while confirming the hypervariable nature of the coding for amino acids (AAs) at position 67 and 68 in the p25 protein. Whereas over 25% of amplicons recovered from susceptible (lacking any resistance gene) plants possessed a non-cysteine AA at position 68, all amplicons recovered from resistant plants possessed cysteine at this position. The presence of the Rz2 gene in bait plants moreover resulted in the recovery of P25-specific amplicons exhibiting a previously undocumented increased incidence for the coding of methionine at AA position 21. The data document on-going virulence development in BNYVV populations to previously-resistant varieties due to changes in P25 and provide a baseline for the analysis of genetic change in the virus population that may accompany the implementation of new resistance genes to manage rhizomania.