{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["14"],"submitter":["Liebe S"],"funding":["Allianz Industrie Forschung"],"pubmed_abstract":["Beet necrotic yellow vein virus (BNYVV) causes rhizomania disease in sugar beet (<i>Beta vulgaris</i>), which is controlled since more than two decades by cultivars harboring the <i>Rz1</i> resistance gene. The development of resistance-breaking strains has been favored by a high selection pressure on the soil-borne virus population. Resistance-breaking is associated with mutations at amino acid positions 67-70 (tetrad) in the RNA3 encoded pathogenicity factor P25 and the presence of an additional RNA component (RNA5). However, natural BNYVV populations are highly diverse making investigations on the resistance-breaking mechanism rather difficult. Therefore, we applied a reverse genetic system for BNYVV (A type) to study <i>Rz1</i> resistance-breaking by direct agroinoculation of sugar beet seedlings. The bioassay allowed a clear discrimination between susceptible and <i>Rz1</i> resistant plants already four weeks after infection, and resistance-breaking was independent of the sugar beet <i>Rz1</i> genotype. A comprehensive screen of natural tetrads for resistance-breaking revealed several new mutations allowing BNYVV to overcome <i>Rz1</i>. The supplementation of an additional RNA5 encoding the pathogenicity factor P26 allowed virus accumulation in the <i>Rz1</i> genotype independent of the P25 tetrad. This suggests the presence of two distinct resistance-breaking mechanisms allowing BNYVV to overcome <i>Rz1</i>. Finally, we showed that the resistance-breaking effect of the tetrad and the RNA5 is specific to <i>Rz1</i> and has no effect on the stability of the second resistance gene <i>Rz2</i>. Consequently, double resistant cultivars (<i>Rz1</i>+<i>Rz2</i>) should provide effective control of <i>Rz1</i> resistance-breaking strains. Our study highlights the flexibility of the viral genome allowing BNYVV to overcome host resistance, which underlines the need for a continuous search for alternative resistance genes."],"journal":["Frontiers in plant science"],"pagination":["1098786"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10102433"],"repository":["biostudies-literature"],"pubmed_title":["The arms race between beet necrotic yellow vein virus and host resistance in sugar beet."],"pmcid":["PMC10102433"],"pubmed_authors":["Varrelmann M","Maiss E","Liebe S"],"additional_accession":[]},"is_claimable":false,"name":"The arms race between beet necrotic yellow vein virus and host resistance in sugar beet.","description":"Beet necrotic yellow vein virus (BNYVV) causes rhizomania disease in sugar beet (<i>Beta vulgaris</i>), which is controlled since more than two decades by cultivars harboring the <i>Rz1</i> resistance gene. The development of resistance-breaking strains has been favored by a high selection pressure on the soil-borne virus population. Resistance-breaking is associated with mutations at amino acid positions 67-70 (tetrad) in the RNA3 encoded pathogenicity factor P25 and the presence of an additional RNA component (RNA5). However, natural BNYVV populations are highly diverse making investigations on the resistance-breaking mechanism rather difficult. Therefore, we applied a reverse genetic system for BNYVV (A type) to study <i>Rz1</i> resistance-breaking by direct agroinoculation of sugar beet seedlings. The bioassay allowed a clear discrimination between susceptible and <i>Rz1</i> resistant plants already four weeks after infection, and resistance-breaking was independent of the sugar beet <i>Rz1</i> genotype. A comprehensive screen of natural tetrads for resistance-breaking revealed several new mutations allowing BNYVV to overcome <i>Rz1</i>. The supplementation of an additional RNA5 encoding the pathogenicity factor P26 allowed virus accumulation in the <i>Rz1</i> genotype independent of the P25 tetrad. This suggests the presence of two distinct resistance-breaking mechanisms allowing BNYVV to overcome <i>Rz1</i>. Finally, we showed that the resistance-breaking effect of the tetrad and the RNA5 is specific to <i>Rz1</i> and has no effect on the stability of the second resistance gene <i>Rz2</i>. Consequently, double resistant cultivars (<i>Rz1</i>+<i>Rz2</i>) should provide effective control of <i>Rz1</i> resistance-breaking strains. Our study highlights the flexibility of the viral genome allowing BNYVV to overcome host resistance, which underlines the need for a continuous search for alternative resistance genes.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023","modification":"2026-06-26T03:08:42.813Z","creation":"2025-04-04T14:30:16.269Z"},"accession":"S-EPMC10102433","cross_references":{"pubmed":["37063189"],"doi":["10.3389/fpls.2023.1098786"]}}