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ARS Home » Pacific West Area » Salinas, California » Crop Improvement and Protection Research » Research » Publications at this Location » Publication #196773
Title: DISTRIBUTION AND MOLECULAR ANALYSIS OF RESISTANCE-BREAKING ISOLATES OF BEET NECROTIC YELLOW VEIN VIRUS IN THE UNITED STATES

Author
item Liu, Hsing Yeh
item Lewellen, Robert

Submitted to: Phytopathology
Publication Type: Abstract Only
Publication Acceptance Date: 6/30/2006
Publication Date: 7/29/2006
Citation: Liu, H., Lewellen, R.T. 2006. Distribution and molecular analysis of resistance-breaking isolates of beet necrotic yellow vein virus in the united states. Phytopathology. 96:S69.

Interpretive Summary: N/A

Technical Abstract: Rhizomania is one of the most economically important diseases of sugar beet. It is caused by Bee necrotic yellow vein virus (BNYVV) and is vectored by the plasmodiophorid Polymyxa betae. The disease can only be controlled effectively by the use of resistant cultivars. In 2003, the resistance-breaking (RB) isolates of BNYVV were identified in the Imperial Valley of California. These isolates do not contain RNA-5 as determined by RT-PCR. From the banding patterns of single-strand conformation polymorphism and sequence analyses we concluded that the RB BNYVV isolates had likely evolved from the original existing A-type. Rhizomania infested sugar beet fields throughout the United States were surveyed in 2004-2005. Our soil survey indicated that the RB isolates not only existed in California but also in Colorado, Idaho, Minnesota, Nebraska, and Oregon. Analyses of the deduced amino acid sequence of coat protein and P-25 protein of RB BNYVV isolates revealed the high percentage of identity with non-RB BNYVV isolates (99.9 percent and >98.0 percent respectively). The variable amino acids in P-25 protein were located at the residues of 67 and 68. In the United States, the two amino acids found in the non-RB isolates were uniques (AC), whereas the RB isolates were variable (AF, AL, SY, VC, VL, or AC). In order to prove that the 67 and 68 amino acid changes in P-25 protein cause the resistance-breaking, the infectious clones will be needed to draw conclusions.