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United States Department of Agriculture

Agricultural Research Service

Title: Distribution and molecular characterization of resistance-breaking isolates of Beet necrotic yellow vein virus in the United States

Authors
item Liu, Hsing Yeh
item Lewellen, Robert

Submitted to: Plant Disease
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 14, 2007
Publication Date: June 26, 2007
Citation: Liu, H., Lewellen, R.T. 2007. Distribution and molecular characterization of resistance-breaking isolates of Beet necrotic yellow vein virus in the United States. Plant Disease. 91:847-851.

Interpretive Summary: Rhizomania is a serious disease of sugar beet. This disease is caused by Beet necrotic yellow vein virus (BNYVV) and vectored by the plasmodiophorid Polymyxa betae. The major problem to control rhizomania disease is that the resting spore of the viruliferous fungal vector is able to survive in the soil for at least 15 years. Hence, use resistant cultivars have been the only economical way to control this devastating disease. Partially resistant sugar beet cultivars based upon single dominant genes have been developed and are widely used by the sugar beet industry. During 2003 and 2004 in the Imperial Valley of California, partially resistant sugar beet cultivars with Rz1 allele seemed to be compromised. Distinct BNYVV isolates have been identified from these plants. 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 resistance-breaking BNYVV isolates from Imperial Valley 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 resistance-breaking isolates not only existed in the Imperial Valley and San Joaquin Valley of California but also in Colorado, Idaho, Minnesota, Nebraska, and Oregon. Out of all the soil samples we tested, 92.5% of 'Beta 6600' (rz1rz1rz1), 77.5% of 'Beta 4430R' (Rz1rz1), 45.0% of 'Beta G017R' (Rz2rz2), and 15.0% of 'KWS Angelina' (Rz1rz1+Rz2rz2) were infected with BNYVV. Analyses of the deduced amino acid sequence of coat protein and P-25 protein of resistance-breaking BNYVV isolates revealed the high percentage of identity with non-resistance-breaking BNYVV isolates (99.9% and >98.0% respectively). The P-25 proteins in all isolates consisted of 219 amino acid residues and there was a maximum of 10 amino acid differences. The variable amino acids in P-25 proteins were located at the residues of 67and 68. In the United States, the two amino acids found in the non-resistance-breaking isolates were conserved (AC). The resistance-breaking isolates were variable including AF, AL, SY, VC, VL, as well as AC. we cannot depend on the change of these two amino acids to absolute differentiate resistance-breaking and non-resistance-breaking isolates of BNYVV.

Technical Abstract: Beet necrotic yellow vein virus (BNYVV) is the causal agent of rhizomania disease of sugar beet (Beta vulgaris L.). The virus is transmitted by the plasmodiophorid Polymyxa betae. The disease can only be controlled effectively by the use of partially resistant cultivars. During 2003 and 2004 in the Imperial Valley of California, partially resistant sugar beet cultivars with Rz1 allele seemed to be compromised. Distinct BNYVV isolates have been identified from these plants. 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 resistance-breaking BNYVV isolates from Imperial Valley 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 resistance-breaking isolates not only existed in the Imperial Valley and San Joaquin Valley of California but also in Colorado, Idaho, Minnesota, Nebraska, and Oregon. Out of all the soil samples we tested, 92.5% of 'Beta 6600' (rz1rz1rz1), 77.5% of 'Beta 4430R' (Rz1rz1), 45.0% of 'Beta G017R' (Rz2rz2), and 15.0% of 'KWS Angelina' (Rz1rz1+Rz2rz2) were infected with BNYVV. Analyses of the deduced amino acid sequence of coat protein and P-25 protein of resistance-breaking BNYVV isolates revealed the high percentage of identity with non-resistance-breaking BNYVV isolates (99.9% and >98.0% respectively). The P-25 proteins in all isolates consisted of 219 amino acid residues and there was a maximum of 10 amino acid differences. The variable amino acids in P-25 proteins were located at the residues of 67and 68. In the United States, the two amino acids found in the non-resistance-breaking isolates were conserved (AC). The resistance-breaking isolates were variable including AF, AL, SY, VC, VL, as well as AC. we cannot depend on the change of these two amino acids to absolute differentiate resistance-breaking and non-resistance-breaking isolates of BNYVV.

Last Modified: 4/17/2014
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