Soybean mosaic virus (SMV; Genus Potyvirus; Family Potyviridae) is one of the most widespread viruses in soybean (Glycine max [L.] Merr.). Hutcheson, a cultivar developed in Virginia, is resistant to the common strains of SMV. However, new resistance-breaking (RB) isolates of SMV have emerged in natural infections to break the resistance of Hutcheson containing the Rsv1y allele. These RB isolates are SMV-G5 and G6-like based on the differential reactions on soybean cultivars with the Rsv1 locus, and are more G6-like based on the amino acid sequence of the coat protein (CP). The CP of the RB isolates is diverse at the amino and carboxy termini and highly conserved in the core region. RB isolates reduce the yield of susceptible cultivars and cause mottling of the seed coat. Dual infection of soybeans with SMV and BPMV increased the severity of symptoms, including plant stunting and SMV titer in comparison to single SMV inoculations. The reactions of Hutcheson and herbicide-tolerant Hutcheson RR were similar with or without herbicide application. Resistance to SMV is controlled by single dominant genes at three distinct loci, Rsv1, Rsv3 and Rsv4. The mechanisms of resistance at the Rsv3 and Rsv4 loci were investigated by tracking virus accumulation and movement over time using leaf immunoprints. The mechanisms of Rsv3 resistance include extreme resistance, hypersensitive response, or restriction to virus replication and movement, which are strain specific. The Rsv4 gene was found to function in a non-strain specific and non-necrotic manner. The mechanisms of Rsv4 resistance involve restricting both cell-to-cell and long distance movement of SMV. The Rsv1, Rsv3 and Rsv4 resistance genes exhibit a continuum of SMV-soybean interactions, and include complete susceptibility, local and systemic necrosis, restriction of virus movement (both cell-to-cell and long distance), reduction in virus accumulation, and extreme resistance with no detectable virus. Cultivars containing two genes for resistance, Rsv1 and Rsv3 or Rsv1 and Rsv4, were resistant to multiple strains of SMV tested and show great potential for gene pyramiding efforts to ensure a wider and more durable resistance to SMV in soybeans. / Ph. D.

The varroa mite is a primary driver behind periodical losses of honey bee colonies. The mite requires bees for food and reproduction and, in turn, elicits physiological deficiencies and diseases that compromise bee colony health. The mite nervous system is a target site for existing acaricides. These acaricides not only have adverse health effects on bees, but resistance limits their use to reduce mites and diseases in bee colonies. Voltage-gated chloride channels are involved in the maintenance of nerve and muscle excitability in arthropod pests, which suggests that these channels might be exploited as targets for acaricides. Apistan® (the pyrethroid tau-fluvalinate), Checkmite+® (the organophosphate coumaphos), and Apivar® (the formamidine amitraz) are control products for mite management. The effectiveness of these chemistries has diminished as a result of the increasing incidence resistance in mite populations. I report a toxicological analysis of stilbene products against acaricide-susceptible and -resistant mites. My results find a significant increase in metabolic detoxification enzyme activities in acaricide-resistant mites compared to susceptible mites. Acetylcholinesterase of coumaphos-resistant mites was significantly less sensitive to the toxic coumaphos metabolite compared to susceptible mites, which suggests target-site insensitivity as a mechanism of acaricide resistance. The stilbene product DIDS had significantly higher field efficacy to acaricide-resistant mites compared to Apistan®- and CheckMite+®. These data suggest that DIDS, and other stilbene products, might serve as candidate chemistries to continue field efficacy testing of alternative acaricides for Apistan® and CheckMite+® resistant mites. / Master of Science in Life Sciences