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Strausbaugh C.a. - One of the best experts on this subject based on the ideXlab platform.
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Commercial sugar beet cultivars evaluated for Rhizomania resistance and storability in Idaho, 2018
2020Co-Authors: Strausbaugh C.a.Abstract:Rhizomania caused by Beet necrotic yellow vein virus (BNYVV) and storage losses are serious sugar beet production problems. To identify sugar beet cultivars with resistance to BNYVV and evaluate storability, 30 commercial cultivars were screened by growing them in a sugar beet field infested with BNYVV in Kimberly, ID during the 2018 growing season in a randomized complete block design with 6 replications. At harvest on 26-27 September 2018, roots were dug and evaluated for symptoms of Rhizomania and also placed in an indoor commercial sugar beet storage building. After 136 days in storage, samples were evaluated for surface rot, weight loss, and sucrose loss. Surface root rot ranged from 17 to 81%, weight loss ranged from 22 to 32%, sucrose losses ranged from 44 to 87%, and estimated recoverable sucrose ranged from 803 to 7,207 lb/A. Given these response ranges, selecting cultivars for Rhizomania resistance and combining this resistance with storability will lead to considerable economic benefit for the sugar beet industry
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Experimental sugar beet cultivars evaluated for Rhizomania resistance and storability in Idaho, 2018
2020Co-Authors: Strausbaugh C.a.Abstract:Rhizomania caused by Beet necrotic yellow vein virus (BNYVV) and storage losses are serious sugar beet production problems. To identify sugar beet cultivars with resistance to BNYVV and evaluate storability, 12 experimental cultivars were screened by growing them in a sugar beet field infested with BNYVV in Kimberly, ID during the 2018 growing season in a randomized complete block design with 6 replications. At harvest on 26-27 September 2018, roots were dug and evaluated for symptoms of Rhizomania and also placed in an indoor commercial sugar beet storage building. After 136 days in storage, samples were evaluated for surface rot, weight loss, and sucrose loss. Surface root rot ranged from 22 to 79%, weight loss ranged from 22 to 32%, sucrose losses ranged from 50 to 82%, and estimated recoverable sucrose ranged from 803 to 6,246 lb/A. Given these response ranges, selecting cultivars for Rhizomania resistance and combining this resistance with storability will lead to considerable economic benefit for the sugar beet industry
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Ft. Collins sugar beet germplasm evaluated for Rhizomania and storage rot resistance in Idaho, 2018
2019Co-Authors: Strausbaugh C.a., Fenwick A.l.Abstract:Rhizomania caused by Beet necrotic yellow vein virus (BNYVV) and storage losses are serious sugar beet production problems. To identify sugar beet germplasm lines with resistance to BNYVV and storage rots, 30 lines from the USDA-ARS Ft. Collins sugar beet program and four check cultivars were screened. The lines were grown in a sugar beet field infested with BNYVV during the 2018 growing season in a randomized complete block design with 6 replications. At harvest on 15 October 2018, roots were dug and evaluated for Rhizomania symptoms and also placed in an indoor commercial sugar beet storage building. After 119 days in storage, samples were evaluated for the percentage of root surface area covered by fungal growth or rot. Rhizomania symptom development in the field was uniform and other disease problems were not evident in the plot area. The BNYVV susceptible check plots had 97% foliar symptoms and high root disease severity ratings. The three resistant checks had 0 to 6% foliar symptoms and low root ratings. Based on root ratings, three entries (4, 13, and 14) had resistance similar to the resistant checks. However, entry 13 (20121018HO-119) was the only entry that performed well for all variables. Entry 13 may serve as a starting point for identifying additional sources of resistance to BNYVV and storage rots
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Experimental sugar beet cultivars evaluated for Rhizomania resistance and storability in Idaho, 2017
2019Co-Authors: Strausbaugh C.a.Abstract:Rhizomania caused by Beet necrotic yellow vein virus (BNYVV) and storage losses are serious sugar beet production problems. To identify sugar beet cultivars with resistance to BNYVV and evaluate storability, 7 experimental cultivars were screened by growing them in a sugar beet field infested with BNYVV in Kimberly, ID during the 2017 growing season in a randomized complete block design with 6 replications. At harvest on 2-3 October 2017, roots were dug and evaluated for symptoms of Rhizomania and also placed in an indoor commercial sugar beet storage building. After 147 days in storage, samples were evaluated for surface rot, weight loss, and sucrose loss. Surface root rot ranged from 16 to 85%, weight loss ranged from 17 to 28%, sucrose losses ranged from 25 to 87%, and estimated recoverable sucrose ranged from 596 to 8,518 lb/A. Given these response ranges, selecting cultivars for Rhizomania resistance and combining this resistance with storability will lead to considerable economic benefit for the sugar beet industry
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Commercial sugar beet cultivars evaluated for Rhizomania resistance and storability in Idaho, 2017.
2019Co-Authors: Strausbaugh C.a.Abstract:Rhizomania caused by Beet necrotic yellow vein virus (BNYVV) and storage losses are serious sugar beet production problems. To identify sugar beet cultivars with resistance to BNYVV and evaluate storability, 26 commercial cultivars were screened by growing them in a sugar beet field infested with BNYVV in Kimberly, ID during the 2017 growing season in a randomized complete block design with 6 replications. At harvest on 2-3 October 2017, roots were dug and evaluated for symptoms of Rhizomania and also placed in an indoor commercial sugar beet storage building. After 147 days in storage, samples were evaluated for surface rot, weight loss, and sucrose loss. Surface root rot ranged from 10 to 85%, weight loss ranged from 14 to 28%, sucrose losses ranged from 25 to 87%, and estimated recoverable sucrose ranged from 596 to 9,111 lb/A. Given these response ranges, selecting cultivars for Rhizomania resistance and combining this resistance with storability will lead to considerable economic benefit for the sugar beet industry
Anne Legrève - One of the best experts on this subject based on the ideXlab platform.
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Long Term Management of Rhizomania Disease-Insight Into the Changes of the Beet necrotic yellow vein virus RNA-3 Observed Under Resistant and Non-resistant Sugar Beet Fields.
Frontiers in plant science, 2018Co-Authors: Yann Galein, Anne Legrève, Claude BragardAbstract:Rhizomania disease, caused by the Beet necrotic yellow vein virus (BNYVV), is considered as one of the major constraints for sugar beet production, worldwide. As a result of the introgression of major resistance genes (Holly, Rz2) in commercially available sugar beet varieties, the virus has endured strong selection pressure since the 90s'. Understanding the virus response and diversity to sugar beet resistance is a key factor for a sustainable management of only few resistance genes. Here we report Rhizomania surveys conducted in a Rhizomania hot spot, the Pithiviers area (France) during a 4-year period and complementary to the study of Schirmer et al. (2005). The study aimed at evaluating the intra- and inter-field BNYVV diversity in response to different sources of resistance and over the growing season. To follow Rhizomania development over the sugar beet growing season, extensive field samplings combined with field assays were performed in this study. The evolution of the BNYVV diversity was assessed at intra- and inter-field levels, with sugar beet cultivars containing different resistance genes (Rz1, Rz1 + Heterodera schachtii resistance and Rz1Rz2). Intra-field diversity was analyzed at the beginning and the end of the growing season of each field. From more than one thousand field samples, the simultaneous presence of the different A, B and P types of BNYVV was confirmed, with 21 variants identified at positions 67-70 of the p25 tetrad. The first variant, AYHR, was found most commonly followed by SYHG. Numerous mixed infections (9.93% of the samples), mostly of B-type with P-type, have also been evidenced. Different tetrads associated with the A- or B-type were also found with a fifth RNA-genome component known to allow more aggressiveness to BNYVV on sugar beet roots. Cultivars with Rz1+Rz2 resistant genes showed few root symptoms even if the BNYVV titre was quite high according to the BNYVV type present. The virus infectious potential in the soil at the end of the growing season with such cultivars was also lower despite a wider diversity at the BNYVV RNA3 sequence level. Rz1+Rz2 cultivars also exhibited a lower presence of Beet soil-borne virus (BSBV), a P. betae-transmitted Pomovirus. Cultivars with Rz1 and nematode (N) resistance genes cultivated in field infected with nematodes showed lower BNYVV titre than those with Rz1 or Rz1+Rz2 cultivars. Overall, the population structure of BNYVV in France is shown to be different from that previously evidenced in different world areas. Implications for long-term management of the resistance to Rhizomania is discussed.
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Long Term Management of Rhizomania Disease—Insight Into the Changes of the Beet necrotic yellow vein virus RNA-3 Observed Under Resistant and Non-resistant Sugar Beet Fields
Frontiers Media S.A., 2018Co-Authors: Yann Galein, Anne Legrève, Claude BragardAbstract:Rhizomania disease, caused by the Beet necrotic yellow vein virus (BNYVV), is considered as one of the major constraints for sugar beet production, worldwide. As a result of the introgression of major resistance genes (Holly, Rz2) in commercially available sugar beet varieties, the virus has endured strong selection pressure since the 90s'. Understanding the virus response and diversity to sugar beet resistance is a key factor for a sustainable management of only few resistance genes. Here we report Rhizomania surveys conducted in a Rhizomania hot spot, the Pithiviers area (France) during a 4-year period and complementary to the study of Schirmer et al. (2005). The study aimed at evaluating the intra- and inter-field BNYVV diversity in response to different sources of resistance and over the growing season. To follow Rhizomania development over the sugar beet growing season, extensive field samplings combined with field assays were performed in this study. The evolution of the BNYVV diversity was assessed at intra- and inter-field levels, with sugar beet cultivars containing different resistance genes (Rz1, Rz1 + Heterodera schachtii resistance and Rz1Rz2). Intra-field diversity was analyzed at the beginning and the end of the growing season of each field. From more than one thousand field samples, the simultaneous presence of the different A, B and P types of BNYVV was confirmed, with 21 variants identified at positions 67–70 of the p25 tetrad. The first variant, AYHR, was found most commonly followed by SYHG. Numerous mixed infections (9.93% of the samples), mostly of B-type with P-type, have also been evidenced. Different tetrads associated with the A- or B-type were also found with a fifth RNA-genome component known to allow more aggressiveness to BNYVV on sugar beet roots. Cultivars with Rz1+Rz2 resistant genes showed few root symptoms even if the BNYVV titre was quite high according to the BNYVV type present. The virus infectious potential in the soil at the end of the growing season with such cultivars was also lower despite a wider diversity at the BNYVV RNA3 sequence level. Rz1+Rz2 cultivars also exhibited a lower presence of Beet soil-borne virus (BSBV), a P. betae-transmitted Pomovirus. Cultivars with Rz1 and nematode (N) resistance genes cultivated in field infected with nematodes showed lower BNYVV titre than those with Rz1 or Rz1+Rz2 cultivars. Overall, the population structure of BNYVV in France is shown to be different from that previously evidenced in different world areas. Implications for long-term management of the resistance to Rhizomania is discussed
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Systemic resistance induced by Bacillus lipopeptides in Beta vulgaris reduces infection by the Rhizomania disease vector Polymyxa betae
Molecular plant pathology, 2012Co-Authors: Nicolas Desoignies, Marc Ongena, Florence Schramme, Anne LegrèveAbstract:The control of Rhizomania, one of the most important diseases of sugar beet caused by the Beet necrotic yellow vein virus, remains limited to varietal resistance. In this study, we investigated the putative action of Bacillus amylolequifaciens lipopeptides in achieving Rhizomania biocontrol through the control of the virus vector Polymyxa betae. Some lipopeptides that are produced by bacteria, especially by plant growth-promoting rhizobacteria, have been found to induce systemic resistance in plants. We tested the impact of the elicitation of systemic resistance in sugar beet through lipopeptides on infection by P. betae. Lipopeptides were shown to effectively induce systemic resistance in both the roots and leaves of sugar beet, resulting in a significant reduction in P. betae infection. This article provides the first evidence that induced systemic resistance can reduce infection of sugar beet by P. betae.
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Rhizomania – what is to be learned from the fields?
2011Co-Authors: Yann Galein, Anne Legrève, François Crutzen, Catherine Nagy, Imane Essalhi, Agnès Champeil, Marc Richard-molard, Hervé Escriou, Claude BragardAbstract:Since the widespread use of Rhizomania partially resistant cultivars, bearing the Rz1 gene along with high yield capacities, multiple Rz1 resistance-breaking events have been reported both in the USA and in Europe. A single mutation from alanine to valine in the p25 hypervariable amino acid tetrad was linked with such resistance breaking (Koenig et al., 2009). Although there are difficulties for determining the effect of virus variation along with the role of other soil-borne pathogens, inoculum densities as well as questions regarding a possible genetic erosion of the resistance enhancer genes, understanding the dynamic of the emergence of resistance breaking isolates as well as evaluating their fitness and ability to spread is of the uttermost importance. Between the 2007 and 2010 sugar beet growing season, Rhizomania affected fields have been surveyed in France, in the Pithiviers region. More than 600 samples were collected both in disease and non-disease expressing areas. Samples were tested for the presence of BNYVV by RT-PCR targeting mostly the p14, p25 and p26 genes. The multiplex RT-PCR (Meunier et al., 2003) was also used to detect the Rhizomania-associated pomoviruses Beet soil-borne virus and Beet virus Q, together with their vector Polymyxa betae. The presence of the Beet black scorch virus was also checked in selected samples. In the frame of a long-term study of Rhizomania, field trials were set up in 2009 and 2010 to follow up the evolution of the disease within a single sugar beet growing seasons. The results confirmed the large presence of BNYVV type B and P in the surveyed areas, with mixed infections in single beets. Conversely to reports from other areas, the canonical p25 A-V mutation was almost not found while the AYHR and SYHG tetrads were frequently detected. The results stressed also the need to set up convergent survey methods to facilitate the exchange of data on viral resistance-breaking isolates.
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Rhizomania what is to be learned from the fields
Proceedings of the Eighth Symposium of the International Working Group on Plant Viruses with Fungal Vectors Louvain-La-Neuve Belgium 6-8 July 2011., 2011Co-Authors: Yann Galein, Anne Legrève, François Crutzen, Catherine Nagy, Imane Essalhi, Agnès Champeil, Hervé Escriou, Marc Richardmolard, Claude BragardAbstract:Since the widespread use of Rhizomania partially resistant cultivars, bearing the Rz1 gene along with high yield capacities, multiple Rz1 resistance-breaking events have been reported both in the USA and in Europe. A single mutation from alanine to valine in the p25 hypervariable amino acid tetrad was linked with such resistance breaking (Koenig et al., 2009). Although there are difficulties for determining the effect of virus variation along with the role of other soil-borne pathogens, inoculum densities as well as questions regarding a possible genetic erosion of the resistance enhancer genes, understanding the dynamic of the emergence of resistance breaking isolates as well as evaluating their fitness and ability to spread is of the uttermost importance. Between the 2007 and 2010 sugar beet growing season, Rhizomania affected fields have been surveyed in France, in the Pithiviers region. More than 600 samples were collected both in disease and non-disease expressing areas. Samples were tested for the presence of BNYVV by RT-PCR targeting mostly the p14, p25 and p26 genes. The multiplex RT-PCR (Meunier et al., 2003) was also used to detect the Rhizomania-associated pomoviruses Beet soil-borne virus and Beet virus Q, together with their vector Polymyxa betae. The presence of the Beet black scorch virus was also checked in selected samples. In the frame of a long-term study of Rhizomania, field trials were set up in 2009 and 2010 to follow up the evolution of the disease within a single sugar beet growing seasons. The results confirmed the large presence of BNYVV type B and P in the surveyed areas, with mixed infections in single beets. Conversely to reports from other areas, the canonical p25 A-V mutation was almost not found while the AYHR and SYHG tetrads were frequently detected. The results stressed also the need to set up convergent survey methods to facilitate the exchange of data on viral resistance-breaking isolates.
Claude Bragard - One of the best experts on this subject based on the ideXlab platform.
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Long Term Management of Rhizomania Disease-Insight Into the Changes of the Beet necrotic yellow vein virus RNA-3 Observed Under Resistant and Non-resistant Sugar Beet Fields.
Frontiers in plant science, 2018Co-Authors: Yann Galein, Anne Legrève, Claude BragardAbstract:Rhizomania disease, caused by the Beet necrotic yellow vein virus (BNYVV), is considered as one of the major constraints for sugar beet production, worldwide. As a result of the introgression of major resistance genes (Holly, Rz2) in commercially available sugar beet varieties, the virus has endured strong selection pressure since the 90s'. Understanding the virus response and diversity to sugar beet resistance is a key factor for a sustainable management of only few resistance genes. Here we report Rhizomania surveys conducted in a Rhizomania hot spot, the Pithiviers area (France) during a 4-year period and complementary to the study of Schirmer et al. (2005). The study aimed at evaluating the intra- and inter-field BNYVV diversity in response to different sources of resistance and over the growing season. To follow Rhizomania development over the sugar beet growing season, extensive field samplings combined with field assays were performed in this study. The evolution of the BNYVV diversity was assessed at intra- and inter-field levels, with sugar beet cultivars containing different resistance genes (Rz1, Rz1 + Heterodera schachtii resistance and Rz1Rz2). Intra-field diversity was analyzed at the beginning and the end of the growing season of each field. From more than one thousand field samples, the simultaneous presence of the different A, B and P types of BNYVV was confirmed, with 21 variants identified at positions 67-70 of the p25 tetrad. The first variant, AYHR, was found most commonly followed by SYHG. Numerous mixed infections (9.93% of the samples), mostly of B-type with P-type, have also been evidenced. Different tetrads associated with the A- or B-type were also found with a fifth RNA-genome component known to allow more aggressiveness to BNYVV on sugar beet roots. Cultivars with Rz1+Rz2 resistant genes showed few root symptoms even if the BNYVV titre was quite high according to the BNYVV type present. The virus infectious potential in the soil at the end of the growing season with such cultivars was also lower despite a wider diversity at the BNYVV RNA3 sequence level. Rz1+Rz2 cultivars also exhibited a lower presence of Beet soil-borne virus (BSBV), a P. betae-transmitted Pomovirus. Cultivars with Rz1 and nematode (N) resistance genes cultivated in field infected with nematodes showed lower BNYVV titre than those with Rz1 or Rz1+Rz2 cultivars. Overall, the population structure of BNYVV in France is shown to be different from that previously evidenced in different world areas. Implications for long-term management of the resistance to Rhizomania is discussed.
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Long Term Management of Rhizomania Disease—Insight Into the Changes of the Beet necrotic yellow vein virus RNA-3 Observed Under Resistant and Non-resistant Sugar Beet Fields
Frontiers Media S.A., 2018Co-Authors: Yann Galein, Anne Legrève, Claude BragardAbstract:Rhizomania disease, caused by the Beet necrotic yellow vein virus (BNYVV), is considered as one of the major constraints for sugar beet production, worldwide. As a result of the introgression of major resistance genes (Holly, Rz2) in commercially available sugar beet varieties, the virus has endured strong selection pressure since the 90s'. Understanding the virus response and diversity to sugar beet resistance is a key factor for a sustainable management of only few resistance genes. Here we report Rhizomania surveys conducted in a Rhizomania hot spot, the Pithiviers area (France) during a 4-year period and complementary to the study of Schirmer et al. (2005). The study aimed at evaluating the intra- and inter-field BNYVV diversity in response to different sources of resistance and over the growing season. To follow Rhizomania development over the sugar beet growing season, extensive field samplings combined with field assays were performed in this study. The evolution of the BNYVV diversity was assessed at intra- and inter-field levels, with sugar beet cultivars containing different resistance genes (Rz1, Rz1 + Heterodera schachtii resistance and Rz1Rz2). Intra-field diversity was analyzed at the beginning and the end of the growing season of each field. From more than one thousand field samples, the simultaneous presence of the different A, B and P types of BNYVV was confirmed, with 21 variants identified at positions 67–70 of the p25 tetrad. The first variant, AYHR, was found most commonly followed by SYHG. Numerous mixed infections (9.93% of the samples), mostly of B-type with P-type, have also been evidenced. Different tetrads associated with the A- or B-type were also found with a fifth RNA-genome component known to allow more aggressiveness to BNYVV on sugar beet roots. Cultivars with Rz1+Rz2 resistant genes showed few root symptoms even if the BNYVV titre was quite high according to the BNYVV type present. The virus infectious potential in the soil at the end of the growing season with such cultivars was also lower despite a wider diversity at the BNYVV RNA3 sequence level. Rz1+Rz2 cultivars also exhibited a lower presence of Beet soil-borne virus (BSBV), a P. betae-transmitted Pomovirus. Cultivars with Rz1 and nematode (N) resistance genes cultivated in field infected with nematodes showed lower BNYVV titre than those with Rz1 or Rz1+Rz2 cultivars. Overall, the population structure of BNYVV in France is shown to be different from that previously evidenced in different world areas. Implications for long-term management of the resistance to Rhizomania is discussed
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Rhizomania – what is to be learned from the fields?
2011Co-Authors: Yann Galein, Anne Legrève, François Crutzen, Catherine Nagy, Imane Essalhi, Agnès Champeil, Marc Richard-molard, Hervé Escriou, Claude BragardAbstract:Since the widespread use of Rhizomania partially resistant cultivars, bearing the Rz1 gene along with high yield capacities, multiple Rz1 resistance-breaking events have been reported both in the USA and in Europe. A single mutation from alanine to valine in the p25 hypervariable amino acid tetrad was linked with such resistance breaking (Koenig et al., 2009). Although there are difficulties for determining the effect of virus variation along with the role of other soil-borne pathogens, inoculum densities as well as questions regarding a possible genetic erosion of the resistance enhancer genes, understanding the dynamic of the emergence of resistance breaking isolates as well as evaluating their fitness and ability to spread is of the uttermost importance. Between the 2007 and 2010 sugar beet growing season, Rhizomania affected fields have been surveyed in France, in the Pithiviers region. More than 600 samples were collected both in disease and non-disease expressing areas. Samples were tested for the presence of BNYVV by RT-PCR targeting mostly the p14, p25 and p26 genes. The multiplex RT-PCR (Meunier et al., 2003) was also used to detect the Rhizomania-associated pomoviruses Beet soil-borne virus and Beet virus Q, together with their vector Polymyxa betae. The presence of the Beet black scorch virus was also checked in selected samples. In the frame of a long-term study of Rhizomania, field trials were set up in 2009 and 2010 to follow up the evolution of the disease within a single sugar beet growing seasons. The results confirmed the large presence of BNYVV type B and P in the surveyed areas, with mixed infections in single beets. Conversely to reports from other areas, the canonical p25 A-V mutation was almost not found while the AYHR and SYHG tetrads were frequently detected. The results stressed also the need to set up convergent survey methods to facilitate the exchange of data on viral resistance-breaking isolates.
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Rhizomania what is to be learned from the fields
Proceedings of the Eighth Symposium of the International Working Group on Plant Viruses with Fungal Vectors Louvain-La-Neuve Belgium 6-8 July 2011., 2011Co-Authors: Yann Galein, Anne Legrève, François Crutzen, Catherine Nagy, Imane Essalhi, Agnès Champeil, Hervé Escriou, Marc Richardmolard, Claude BragardAbstract:Since the widespread use of Rhizomania partially resistant cultivars, bearing the Rz1 gene along with high yield capacities, multiple Rz1 resistance-breaking events have been reported both in the USA and in Europe. A single mutation from alanine to valine in the p25 hypervariable amino acid tetrad was linked with such resistance breaking (Koenig et al., 2009). Although there are difficulties for determining the effect of virus variation along with the role of other soil-borne pathogens, inoculum densities as well as questions regarding a possible genetic erosion of the resistance enhancer genes, understanding the dynamic of the emergence of resistance breaking isolates as well as evaluating their fitness and ability to spread is of the uttermost importance. Between the 2007 and 2010 sugar beet growing season, Rhizomania affected fields have been surveyed in France, in the Pithiviers region. More than 600 samples were collected both in disease and non-disease expressing areas. Samples were tested for the presence of BNYVV by RT-PCR targeting mostly the p14, p25 and p26 genes. The multiplex RT-PCR (Meunier et al., 2003) was also used to detect the Rhizomania-associated pomoviruses Beet soil-borne virus and Beet virus Q, together with their vector Polymyxa betae. The presence of the Beet black scorch virus was also checked in selected samples. In the frame of a long-term study of Rhizomania, field trials were set up in 2009 and 2010 to follow up the evolution of the disease within a single sugar beet growing seasons. The results confirmed the large presence of BNYVV type B and P in the surveyed areas, with mixed infections in single beets. Conversely to reports from other areas, the canonical p25 A-V mutation was almost not found while the AYHR and SYHG tetrads were frequently detected. The results stressed also the need to set up convergent survey methods to facilitate the exchange of data on viral resistance-breaking isolates.
William M. Wintermantel - One of the best experts on this subject based on the ideXlab platform.
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Registration of FC1740 and FC1741 Multigerm, Rhizomania‐Resistant Sugar Beet Germplasm with Resistance to Multiple Diseases
Journal of Plant Registrations, 2018Co-Authors: Lee Panella, William M. Wintermantel, Imad A. Eujayl, Carl A. Strausbaugh, Kelley L. Richardson, Ann L. Fenwick, Piergiorgio Stevanato, R. T. LewellenAbstract:FC1740 (Reg No. GP-293, PI 681717) and FC1741 (Reg No. GP-294, PI 681718) sugar beet germplasm (Beta vulgaris L.) were developed by the USDA-ARS at Fort Collins, CO, Salinas, CA, and Kimberly, ID, in cooperation with the Beet Sugar Development Foundation, Denver, CO. These germplasm are diploid, multigerm sugar beet populations in normal cytoplasm, segregating for self-sterility (Sf:SsSs), genetic male sterility (A:aa), and hypocotyl color (R:rr). FC1740 and FC1741 have excellent resistance to Rhizomania (Beet necrotic yellow vein virus). FC1740 was selected as homozygous resistant to markers linked to both Rz1 and Rz2 genes for Rhizomania resistance. FC1741 was selected as homozygous to the marker linked to the Rz2 gene for resistance. Both germplasm also have resistance to beet curly top (Beet curly top virus) and Fusarium yellows (Fusarium oxysporum Schlechtend.:Fr. f. sp. betae (D. Stewart) W. C. Snyder & H. N. Hans. and other Fusarium spp.), as well as moderate resistance to Aphanomyces root rot (Aphanomyces cochlioides Drechs.). Neither line exhibited resistance to Cercospora leaf spot (Cercospora beticola Sacc.), Rhizoctonia crown and root rot (Rhizoctonia solani Kuhn.) or sugar beet root aphid (Pemphigus spp.). These germplasm provide sources from which to select disease-resistant, multigerm pollinator parents with either or both of the Rz1 and Rz2 sources of Rhizomania resistance. Because they are from the same population, they also are useful as controls of known genetic background in comparing entries screened for Rhizomania resistance conditioned by Rz1 or Rz2.
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Interactions Between Beet necrotic yellow vein virus and Beet soilborne mosaic virus in Sugar Beet
Plant Disease, 2003Co-Authors: Gail C. Wisler, R. T. Lewellen, J. L. Sears, J. W. Wasson, H.-y. Liu, William M. WintermantelAbstract:Soils naturally infested with cultures of aviruliferous Polymyxa betae and viruliferous P. betae carrying two sugar beet benyviruses, Beet necrotic yellow vein virus (BNYVV) and Beet soilborne mosaic virus (BSBMV), alone and in combination, were compared with noninfested soil for their effects on seedling emergence, plant fresh weight, and virus content as measured by enzyme-linked immunosorbent assay (ELISA). Studies examined sugar beet with and without resistance to the disease Rhizomania, caused by BNYVV. The Rz gene, conferring resistance to BNYVV, did not confer resistance to BSBMV. BSBMV ELISA values were significantly higher in single infections than in mixed infections with BNYVV, in both the Rhizomania-resistant and -susceptible cultivars. In contrast, ELISA values of BNYVV were high (8 to 14 times the healthy mean) in single and mixed infections in the Rhizomania-susceptible cultivar, but were low (approximately three times the healthy mean) in the Rhizomania-resistant cultivar. Results indicate BNYVV may suppress BSBMV in mixed infections, even in Rhizomania-resistant cultivars in which ELISA values for BNYVV are extremely low. Soils infested with P. betae, and with one or both viruses, showed significantly reduced fresh weight of seedlings, and aviruliferous P. betae significantly decreased sugar beet growth in assays.
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First Report of Rhizomania Disease of Sugar Beet Caused by Beet necrotic yellow vein virus in the Great Lakes Production Region.
Plant disease, 2003Co-Authors: William M. Wintermantel, Teresa Crook, Ralph FoggAbstract:Rhizomania, caused by Beet necrotic yellow vein virus (BNYVV) and vectored by the soilborne fungus Polymyxa betae Keskin, is one of the most economically damaging diseases affecting sugar beet (Beta vulgaris L.). The virus likely originated in Europe and was first identified in California in 1983 (1). It has since spread among American sugar beet production regions in spite of vigorous sanitation efforts, quarantine, and disease monitoring (3). In the fall of 2002, mature sugar beet plants exhibiting typical Rhizomania root symptoms, including proliferation of hairy roots, vascular discoloration, and some root constriction (2) were found in several fields scattered throughout central and eastern Michigan. Symptomatic beets were from numerous cultivars, all susceptible to Rhizomania. Two to five sugar beet root samples were collected from each field and sent to the USDA-ARS in Salinas, CA for analysis. Hairy root tissue from symptomatic plants was used for mechanical inoculation of indicator plants. Mechan...
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First Report of Rhizomania of Sugar Beet in the Columbia River Basin of Washington and Oregon.
Plant disease, 2002Co-Authors: John J. Gallian, William M. Wintermantel, Philip B. HammAbstract:Rhizomania, caused by Beet necrotic yellow vein virus (BNYVV) and vectored by the soilborne fungus, Polymyxa betae Keskin, is one of the most economically damaging diseases affecting sugar beet (Beta vulgaris L.) worldwide and has been found in most sugar beet-growing areas of the United States (2). During harvest in October 2000, sugar beet plants exhibiting typical symptoms of Rhizomania (1) were found in a field near Paterson, WA. Sugar beet had been planted in the field in 1999 and 2000, but prior to this, the field had not been planted with sugar beet for approximately 20 years. Symptomatic roots from the field exhibited stunting, vascular discoloration, and proliferation of lateral rootlets. Leaves of affected plants were chlorotic. Four soil samples were taken from symptomatic areas of the field and diluted with an equal amount of sterile sand. Seeds of Rhizomania-susceptible sugar beet cv. Beta 8422 were planted in the soil and sand mix and maintained in a controlled environment at 24°C and 12 h o...
Yann Galein - One of the best experts on this subject based on the ideXlab platform.
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Long Term Management of Rhizomania Disease-Insight Into the Changes of the Beet necrotic yellow vein virus RNA-3 Observed Under Resistant and Non-resistant Sugar Beet Fields.
Frontiers in plant science, 2018Co-Authors: Yann Galein, Anne Legrève, Claude BragardAbstract:Rhizomania disease, caused by the Beet necrotic yellow vein virus (BNYVV), is considered as one of the major constraints for sugar beet production, worldwide. As a result of the introgression of major resistance genes (Holly, Rz2) in commercially available sugar beet varieties, the virus has endured strong selection pressure since the 90s'. Understanding the virus response and diversity to sugar beet resistance is a key factor for a sustainable management of only few resistance genes. Here we report Rhizomania surveys conducted in a Rhizomania hot spot, the Pithiviers area (France) during a 4-year period and complementary to the study of Schirmer et al. (2005). The study aimed at evaluating the intra- and inter-field BNYVV diversity in response to different sources of resistance and over the growing season. To follow Rhizomania development over the sugar beet growing season, extensive field samplings combined with field assays were performed in this study. The evolution of the BNYVV diversity was assessed at intra- and inter-field levels, with sugar beet cultivars containing different resistance genes (Rz1, Rz1 + Heterodera schachtii resistance and Rz1Rz2). Intra-field diversity was analyzed at the beginning and the end of the growing season of each field. From more than one thousand field samples, the simultaneous presence of the different A, B and P types of BNYVV was confirmed, with 21 variants identified at positions 67-70 of the p25 tetrad. The first variant, AYHR, was found most commonly followed by SYHG. Numerous mixed infections (9.93% of the samples), mostly of B-type with P-type, have also been evidenced. Different tetrads associated with the A- or B-type were also found with a fifth RNA-genome component known to allow more aggressiveness to BNYVV on sugar beet roots. Cultivars with Rz1+Rz2 resistant genes showed few root symptoms even if the BNYVV titre was quite high according to the BNYVV type present. The virus infectious potential in the soil at the end of the growing season with such cultivars was also lower despite a wider diversity at the BNYVV RNA3 sequence level. Rz1+Rz2 cultivars also exhibited a lower presence of Beet soil-borne virus (BSBV), a P. betae-transmitted Pomovirus. Cultivars with Rz1 and nematode (N) resistance genes cultivated in field infected with nematodes showed lower BNYVV titre than those with Rz1 or Rz1+Rz2 cultivars. Overall, the population structure of BNYVV in France is shown to be different from that previously evidenced in different world areas. Implications for long-term management of the resistance to Rhizomania is discussed.
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Long Term Management of Rhizomania Disease—Insight Into the Changes of the Beet necrotic yellow vein virus RNA-3 Observed Under Resistant and Non-resistant Sugar Beet Fields
Frontiers Media S.A., 2018Co-Authors: Yann Galein, Anne Legrève, Claude BragardAbstract:Rhizomania disease, caused by the Beet necrotic yellow vein virus (BNYVV), is considered as one of the major constraints for sugar beet production, worldwide. As a result of the introgression of major resistance genes (Holly, Rz2) in commercially available sugar beet varieties, the virus has endured strong selection pressure since the 90s'. Understanding the virus response and diversity to sugar beet resistance is a key factor for a sustainable management of only few resistance genes. Here we report Rhizomania surveys conducted in a Rhizomania hot spot, the Pithiviers area (France) during a 4-year period and complementary to the study of Schirmer et al. (2005). The study aimed at evaluating the intra- and inter-field BNYVV diversity in response to different sources of resistance and over the growing season. To follow Rhizomania development over the sugar beet growing season, extensive field samplings combined with field assays were performed in this study. The evolution of the BNYVV diversity was assessed at intra- and inter-field levels, with sugar beet cultivars containing different resistance genes (Rz1, Rz1 + Heterodera schachtii resistance and Rz1Rz2). Intra-field diversity was analyzed at the beginning and the end of the growing season of each field. From more than one thousand field samples, the simultaneous presence of the different A, B and P types of BNYVV was confirmed, with 21 variants identified at positions 67–70 of the p25 tetrad. The first variant, AYHR, was found most commonly followed by SYHG. Numerous mixed infections (9.93% of the samples), mostly of B-type with P-type, have also been evidenced. Different tetrads associated with the A- or B-type were also found with a fifth RNA-genome component known to allow more aggressiveness to BNYVV on sugar beet roots. Cultivars with Rz1+Rz2 resistant genes showed few root symptoms even if the BNYVV titre was quite high according to the BNYVV type present. The virus infectious potential in the soil at the end of the growing season with such cultivars was also lower despite a wider diversity at the BNYVV RNA3 sequence level. Rz1+Rz2 cultivars also exhibited a lower presence of Beet soil-borne virus (BSBV), a P. betae-transmitted Pomovirus. Cultivars with Rz1 and nematode (N) resistance genes cultivated in field infected with nematodes showed lower BNYVV titre than those with Rz1 or Rz1+Rz2 cultivars. Overall, the population structure of BNYVV in France is shown to be different from that previously evidenced in different world areas. Implications for long-term management of the resistance to Rhizomania is discussed
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Rhizomania – what is to be learned from the fields?
2011Co-Authors: Yann Galein, Anne Legrève, François Crutzen, Catherine Nagy, Imane Essalhi, Agnès Champeil, Marc Richard-molard, Hervé Escriou, Claude BragardAbstract:Since the widespread use of Rhizomania partially resistant cultivars, bearing the Rz1 gene along with high yield capacities, multiple Rz1 resistance-breaking events have been reported both in the USA and in Europe. A single mutation from alanine to valine in the p25 hypervariable amino acid tetrad was linked with such resistance breaking (Koenig et al., 2009). Although there are difficulties for determining the effect of virus variation along with the role of other soil-borne pathogens, inoculum densities as well as questions regarding a possible genetic erosion of the resistance enhancer genes, understanding the dynamic of the emergence of resistance breaking isolates as well as evaluating their fitness and ability to spread is of the uttermost importance. Between the 2007 and 2010 sugar beet growing season, Rhizomania affected fields have been surveyed in France, in the Pithiviers region. More than 600 samples were collected both in disease and non-disease expressing areas. Samples were tested for the presence of BNYVV by RT-PCR targeting mostly the p14, p25 and p26 genes. The multiplex RT-PCR (Meunier et al., 2003) was also used to detect the Rhizomania-associated pomoviruses Beet soil-borne virus and Beet virus Q, together with their vector Polymyxa betae. The presence of the Beet black scorch virus was also checked in selected samples. In the frame of a long-term study of Rhizomania, field trials were set up in 2009 and 2010 to follow up the evolution of the disease within a single sugar beet growing seasons. The results confirmed the large presence of BNYVV type B and P in the surveyed areas, with mixed infections in single beets. Conversely to reports from other areas, the canonical p25 A-V mutation was almost not found while the AYHR and SYHG tetrads were frequently detected. The results stressed also the need to set up convergent survey methods to facilitate the exchange of data on viral resistance-breaking isolates.
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Rhizomania what is to be learned from the fields
Proceedings of the Eighth Symposium of the International Working Group on Plant Viruses with Fungal Vectors Louvain-La-Neuve Belgium 6-8 July 2011., 2011Co-Authors: Yann Galein, Anne Legrève, François Crutzen, Catherine Nagy, Imane Essalhi, Agnès Champeil, Hervé Escriou, Marc Richardmolard, Claude BragardAbstract:Since the widespread use of Rhizomania partially resistant cultivars, bearing the Rz1 gene along with high yield capacities, multiple Rz1 resistance-breaking events have been reported both in the USA and in Europe. A single mutation from alanine to valine in the p25 hypervariable amino acid tetrad was linked with such resistance breaking (Koenig et al., 2009). Although there are difficulties for determining the effect of virus variation along with the role of other soil-borne pathogens, inoculum densities as well as questions regarding a possible genetic erosion of the resistance enhancer genes, understanding the dynamic of the emergence of resistance breaking isolates as well as evaluating their fitness and ability to spread is of the uttermost importance. Between the 2007 and 2010 sugar beet growing season, Rhizomania affected fields have been surveyed in France, in the Pithiviers region. More than 600 samples were collected both in disease and non-disease expressing areas. Samples were tested for the presence of BNYVV by RT-PCR targeting mostly the p14, p25 and p26 genes. The multiplex RT-PCR (Meunier et al., 2003) was also used to detect the Rhizomania-associated pomoviruses Beet soil-borne virus and Beet virus Q, together with their vector Polymyxa betae. The presence of the Beet black scorch virus was also checked in selected samples. In the frame of a long-term study of Rhizomania, field trials were set up in 2009 and 2010 to follow up the evolution of the disease within a single sugar beet growing seasons. The results confirmed the large presence of BNYVV type B and P in the surveyed areas, with mixed infections in single beets. Conversely to reports from other areas, the canonical p25 A-V mutation was almost not found while the AYHR and SYHG tetrads were frequently detected. The results stressed also the need to set up convergent survey methods to facilitate the exchange of data on viral resistance-breaking isolates.