Breakdown of sugar beet Rz1-mediated resistance against Beet necrotic yellow vein virus (BNYVV) infection was previously found, by reverse genetics, to be caused by a single mutation in its p25 gene. The possibility of alternative breaking mutations, however, has not been discarded. To explore the natural diversity of BNYVV in the field and its effects on overcoming Rz1, wild-type (WT) and resistance-breaking (RB) p25 genes from diverse production regions of North America were characterized. The relative titer of WT p25 was inversely correlated with disease expression in Rz1 plants from Minnesota and California. In Minnesota, the predominant WT p25 encoded the A(67)C(68) amino acid signature whereas, in California, it encoded A(67)L(68). In both locations, these WT signatures were associated with asymptomatic BNYVV infections of Rz1 cultivars. Further analyses of symptomatic resistant plants revealed that, in Minnesota, WT A(67)C(68) was replaced by V(67)C(68) whereas, in California, WT A(67)L(68) was replaced by V(67)L(68). Therefore, V(67) was apparently critical in overcoming Rz1 in both pathosystems. The greater genetic distances between isolates from different geographic regions rather than between WT and RB from the same location indicate that the underlying C to U transition originated independently in both BNYVV lineages.

Mite-vectored virus diseases of wheat are common throughout the Great Plains and cause significant economic losses to growers each year. These diseases are caused by Wheat streak mosaic virus (WSMV), Triticum mosaic virus (TriMV), and Wheat mosaic virus (WMoV), all of which are transmitted by the wheat curl mite (WCM), Aceria tosichella Keifer. New wheat cultivars with tolerance or resistance to WSMV have been released recently, but their widespread cultivation and potential impact on mite-transmitted virus incidence in the Texas Panhandle was unknown. A total of 648 symptomatic wheat samples were collected from 26 counties, predominately in the Texas Panhandle, and tested by enzyme-linked immunosorbent assay (ELISA) for WSMV, TriMV, and WMoV. Samples that tested negative by ELISA were subsequently tested by real-time quantitative PCR (qPCR) for each virus. Approximately 93% of the samples tested by ELISA were positive for WSMV, 43% were positive for TriMV, and 7% were positive for WMoV. Eleven samples tested positive only for TriMV, but none were positive only for WMoV. When samples that tested negative for the different viruses by ELISA were retested by real-time qPCR, detection of each virus was significantly increased. When results of the ELISA test and qPCR were combined, 100% of the 648 samples tested positive for WSMV, approximately 94% were positive for TriMV, and 23% were positive for WMoV. This demonstrated that the incidence of TriMV in the Texas High Plains is much greater than previously reported. The fact that real-time qPCR revealed over a 2-fold increase in the incidence of TriMV and a 3-fold increase in WMoV demonstrated that the ELISA test, which is commonly used by diagnostic laboratories in the Great Plains, should not be used for studies requiring a high degree of sensitivity and accuracy in virus detection. After initial virus infection status was determined, samples that tested positive for WSMV and TriMV were further observed for WCM infestation. A total of 292 samples were inspected and a total of 101 mites were collected from 40 tillers. Individual mites and the tillers from which they were recovered were tested by real-time qPCR to determine how copy numbers of WSMV and TriMV in mites and host tissue compared, and whether the WSMV/TriMV copy number ratio in individual mites was similar to that of the host tissue from which they were collected. In all mites and tillers tested, the WSMV copy number was always higher than that of TriMV and copy numbers of both viruses were always higher in plant tissue than in mites. Although there was a significant correlation between the WSMV/TriMV copy number ratio in plant tissue and in associated mites, the correlation coefficient was very low (r = 0.31, P = 0.0248). In the majority of comparisons, the WSMV/TriMV ratio was higher in individual mites than in the tiller from which they were recovered. The reason for this increase is unknown but indicates that mites may preferentially acquire WSMV from tillers coinfected with WSMV and TriMV, a finding that could have significant implications for virus transmission and disease epidemiology.

Theoretical models predict that, under restrictive host conditions, virus populations will exhibit greater genetic variability. This virus response has been experimentally demonstrated in a few cases but its relation with a virus's capability to overcome plant resistance is unknown. To explore the genetic host effects on Beet necrotic yellow vein virus (BNYVV) populations that might be related to resistance durability, a wild-type virus isolate was vector inoculated into partially resistant Rz1, Rz2, and susceptible sugar beet cultivars during a serial planting experiment. Cloning and sequencing a region of the viral RNA-3, involving the pathogenic determinant p25, revealed that virus diversity significantly increased in direct proportion to the strength of host resistance. Thus, whereas virus titers were highest, intermediate, and lowest in susceptible, Rz1, and Rz2 plants, respectively; the average number of nucleotide differences among single-plant populations was 0.8 (±0.1) in susceptible, 1.4 (±0.1) in Rz1, and 2.4 (±0.2) in Rz2 genotypes. A similar relationship between host restriction to BNYVV root accumulation and virus genetic variability was detected in fields of sugar beet where these specific Rz1- and Rz2-mediated resistances have been defeated.

(1) Background: The wheat curl mite (Aceria tosichella Keifer) is a key pest of wheat (Triticum aestivum L.) worldwide. While a number of wheat cultivars resistant to the mites have been employed to minimize the impact on the yield and quality of grain, little is known regarding the mechanisms underlying host plant resistance. Therefore, the goal of this study was to explore changes in transcriptome of resistant and susceptible wheat in order to quantify the molecular changes that drive host plant resistance. (2) Methods: Two varieties, wheat curl mite-susceptible (Karl 92) and wheat curl mite-resistant (TAM112) wheat, both at 2-week postemergence, were used in this study. Half of the plants were exposed to wheat curl mite herbivory and half remained mite-free and served as controls. Transcriptome changes were quantified using RNA-seq and compared among treatments to identify genes and pathways affected by herbivores. (3) Results: We identified a number of genes and pathways involved in plant defenses against pathogens, herbivores, and abiotic stress that were differentially expressed in the resistant wheat exposed to wheat curl mite herbivory but were unaffected in the susceptible wheat. (4) Conclusions: Our outcomes indicated that resistant wheat counteracts wheat curl mite exposure through effective induction of genes and pathways that enhance its defense responses.

Abstract:Around 10 years after the massive deployment of commercial sugarbeet varieties encoding the Rz1 allele, which confers partial dominant resistance to Beet necrotic yellow vein virus (BNYVV) infection, the emergence of resistant breaking (RB) variants of BNYVV was verified in the Imperial Valley of California. Preliminary data suggest that breakdown of Rz1-mediated resistance is also occurring in other production regions of North America. Genetic sequencing of the viral RNA 3, encoding the pathogenic determinant p25 gene, revealed a strong correlation between its amino acid motifs and type of plant virus interaction (i.e., in this case, compatible = disease and incompatible = asymptomatic infection) in the 'Imperial Valley' pathosystem. Thus, most plants from yellow spots in the field and with severe symptoms of rhizomania were infected by virus haplotypes encoding the V 67 L 68 E 135 p25 motif. By contrast, most asymptomatic plants outside the yellow spots were infected by virus haplotypes encoding the avirulent A 67 L 68 D 135 or less frequently by the nationwide wild type A 67 C 68 D 135 motifs. This specific evolutionary trajectory of BNYVV from wild type to RB genotypes apparently was favored under the Imperial Valley conditions. An alternative evolutionary trajectory was found in Minnesota, where wild type A 67 C 68 D 135 evolved directly into an RB variant encoding V 67 C 68 D 135 . These observations demonstrate that the replacement of alanine by valine at position 67 of p25 is critical to overcome Rz1-mediated sugarbeet resistance under natural conditions. Introduction: