Brief Summary of Minutes of Annual Meeting

Please see attached file.

>>>Resistance Definitions A major portion of WERA060 effort has been devoted to developing and reviewing “Resistance Definitions” that can be applied to insecticides, miticides, fungicides, and herbicides. The following draft was prepared: -A- acquired resistance – Resistance to a pesticide in a population acquired through the long-term exposure of the pest to sub-lethal doses over multiple pest generations. altered target-site resistance – Tolerance to a pesticide due to a genetic change leading to an alteration in the target enzyme, protein, or molecule that leads to reduced or no binding of the pesticide. artificially-induced resistance – The development of resistance to a pesticide caused by the deliberate exposure of the pest to sub-lethal doses of a pesticide. -B- baseline sensitivity – A profile of the fungicide sensitivity of a target fungal population based on biological or molecular techniques to assess the response of previously unexposed individual populations to the fungicide of interest. behavioral resistance – Reduced effectiveness of pesticides caused by behavioral changes in a insect pest such as avoidance of pesticide treated hosts; not a result of direct biochemical changes of the organism to the pesticide at the cellular level. biotype – An individual or group of individuals within a particular species having biological traits that are not common to the population as a whole. -C- continuous resistance – The establishment of stable pest populations that are biochemically resistant to a pesticide. This may also refer to the pattern of resistance development in populations where a continuous, quantitative range of sensitivity values can be detected. See directional resistance, quantitative resistance. correlated-resistance – Individuals resistant to one type of pesticide are also resistant to another pesticide with a different biochemical mode of action or target site. See also multiple resistance. cross-resistance – Resistance to multiple pesticides that share the same biochemical mode of action or target site. -D- detoxification mechanisms – A process or processes by which a fungicide is detoxified before the active ingredient reaches the target site. Several different biochemical mechanisms may occur which result in the fungicide being detoxified. The biochemical mechanisms can generally be classified as either: conjugation, hydroloysis, oxidation, or reduction. This can also be referred to as metabolism, see metabolic resistance. directional resistance –A unimodal pattern of resistance development where selection within a population with a continuous, quantitative range in pesticide sensitivity results in an increased frequency of individuals with lower pesticide sensitivity (e.g. the population distribution shifts directionally towards a higher frequency of less sensitive individuals, but the distribution remains a continuous range of pesticide sensitivity). Typically, increased rates of a specific pesticide or using a pesticide with higher inherent activity can provide some control of the population under field conditions. See also continuous resistance, quantitative resistance. discontinuous resistance – A bimodal pattern of resistance development where selection of a population results in the increased frequency of individuals greatly insensitive to the pesticide, usually caused by a target site mutation. See also qualitative resistance, discrete resistance, disruptive resistance. discrete resistance – See qualitative resistance. disruptive resistance – See qualitative resistance. -E- efflux mechanisms – Specific to antibiotic resistance mechanisms within bacterial cells. A method responsible for toxin or antibiotic extrusion outside of a bacterial cell. See intrinsic or acquired resistance. -F- field resistance – A situation where the frequency of resistant individuals in a given pest population is high enough (due to repeated selection events) so that the effectiveness of the pesticide application is compromised such that decreased control is noticed in the field. See also practical resistance. field-evolved resistance – Resistance development in pests in response to field applications of pesticide(s) where repeated use results in the selection of naturally-tolerant individuals to a frequency where control with pesticide(s) is compromised. See practical resistance. fitness – The ability of a pest to naturally reproduce. A pest is often described as having a loss of fitness, or reduced, or increased fitness in the presence of a certain selection pressure, often the presence or absence of a pesticide. forma specialis (f.sp.) – a subspecies or group of strains within a fungal species that can only infect plants within a particular (range of) species, e.g., Puccinia graminis f.sp. tritici. -H- haplotype – A set of DNA polymorphisms, or variations, that tend to be inherited together from a single parent. heteroplasmy – The presence of more than one mitochondrial DNA (mtDNA) within a cell whereby some mutant DNA and wild type DNA is present within the single cell. hormoligosis – The effect of stimulating pest activity through exposure to sub-lethal doses of pesticides; may also be related to the stimulation of pest activity from non-target effects (i.e. increasing pathogen activity with insecticide applications). -I- immunity – Describes a situation where an individual has a mutation that causes the target site to no longer bind to the pesticide, or at such a low level that commercially useable doses of pesticides are ineffective for control. insensitivity – The development of biochemical immunity to a pesticide. See resistance. intrinsic activity – The inhibitory activity of a fungicide against a given species of plant pathogens, based on its ability to bind to the target and to confer growth inhibition, independent of environmental factors that affect its activity, and of the possibility of the selection of individuals that have developed resistance against the fungicide. isolate – A pure culture of a particular organism such as a fungus. Often requires single spore isolation or bacterial colonies from a single cell to have as much genetic homogeneity as possible. -L- laboratory resistance – Selection of resistant pests through repeated pesticide exposure under controlled conditions. This may entail using mutagens to create mutants followed by selection using pesticides. Resistant pests created in this manner may or may not reflect genetic mutations that would survive under natural conditions. The term laboratory resistance is also used to describe resistance phenotypes of field strains that have been described in laboratory assays. Depending on their degree of resistance and their frequency in the field, strains with laboratory resistance might or might not result in field resistance of the fungal population. low-level resistance – The development of tolerance to low doses of a pesticide that may not be significant relative to the rates or doses of pesticides used for commercial pest control. -M- major gene resistance – Resistance associated with changes to a single gene. With known cases the gene affects the pesticide binding ability to the target molecule, protein or enzyme. Typically associated with a target site mutation that confers resistance to the pesticide. major resistance – Pest resistance associated with high economic or biological impact. mechanism of action – See mode of action. mechanism of resistance – The process by which a pest become biochemically resistant to pesticide. Processes are typically related to target site mutations, decreased binding to the target a site, increased gene expression, detoxification or degradation of the pesticide, or efflux of the pesticide away from the target site. This may also refer to the selection process for pest populations and the patterns of increased frequencies of resistant individuals in response to pesticide use strategies. metabolic resistance – Biochemical resistance development based on detoxification or degradation of the pesticide, or efflux of the pesticide away from the target site; e.g. where the target site remains susceptible to pesticide binding but where binding of the pesticide to the target is reduced by other cellular processes. mixed function oxidases – insect enzymes involved in metabolizing insecticides thereby imparting resistance to the pest. mode of action – The biological process by which a pesticide specifically inhibits (biochemical mode of action) the development of a given pest. For example, the biochemical mode of action of QoIs is through the inhibition of cellular respiration. See also target site of action, which describes the exact location of a molecule where a pesticide binds. This may also describe the temporal and spatial characteristics of a pesticide in inhibiting the life or infection cycle of a pest (physical mode of action). For example, QoIs are strongest at inhibiting spore germination and infection processes and have a “protectant” mode of action. multidrug resistance (MDR) – A resistance mechanism based on increased drug efflux, leading to simultaneously reduced sensitivity against several fungicides. Widely observed in European Botrytis cinerea populations from fungicide-treated vineyards and small fruit fields. The major MDR type, MDR1, leads to reduced sensitivity to fludioxonil and anilinopyrimidines, due to mutations in the transcription factor Mrr1 that lead to overexpression of the ABC transporter encoding gene, atrB. MDR2 is caused by overexpression of the MfsM2 transporter triggered by promoter rearrangements, and confers reduced sensitivity to fenhexamid, anilinopyrimidines and iprodione. MDR3 refers to strains expressing both MDR1 and MDR2. Recently, MDR-related mechanisms have been shown to contribute to azole resistance in Mycosphaerella graminicola. multi-step resistance – This refers to the pattern of selection in a population with a continuous distribution of sensitivities to a given pesticide, and when resistance to the same fungicide class is conferred by more than one target site mutation or genetic mechanism. Each of the mutations or mechanisms gives an additive effect. Individuals with a single or a few mutations may have a moderately tolerant phenotype, and those with multiple mutations or mechanisms may have a highly tolerant phenotype. This may also be referred to as “multigenic” resistance. Repeated applications of the pesticide selects for increasingly tolerant individuals and is dependent on the dose of pesticide used, e.g. low doses select out the most sensitive individuals within the population allowing for the survival of moderately sensitive individuals whereas higher doses select out low and moderately sensitive individuals. Very high doses may have a neutral overall effect on the pest, as the dose is so high that even the least sensitive individuals are still controlled. DMI fungicide resistance is a good example of this phenomenon. See also qualitative resistance, and quantitative resistance. multiple resistance – Biochemical resistance development to two or more unrelated pesticide classes. This may result from selection of individuals naturally resistant to two or more pesticides or the sequential selection of individuals resistant to one pesticide class which then naturally obtain a mutation conferring resistance to another pesticide and are subsequently selected for by the use of the latter pesticide. -N- negative cross-resistance – A situation where a pesticide only affects individuals resistant to another class of pesticides. An example is the N-phenylanilines, which are only toxic to individuals that are benzimidazole resistant and ineffective against benzimidazole sensitive individuals. Note that multiple resistance can develop to both pesticides, such in the previous case where an adjacent target site mutation in beta-tubulin also confers resistance to N-phenylanilines in benzimidazole resistant individuals. -O- overexpression – Excessive expression of a particular gene by producing too much of its product or effect. This can lead to a reduction in sensitivity to fungicides in specific fungal systems (e.g., Blumeria jaapii, Fusarium graminearum, Monilinia fructicola, Penicillium digitatum, Sclerotinia homoeocarpa) and a reduction in sensitivity to antibiotics in specific bacterial systems. -P- partial cross-resistance – A situation where biochemical resistance to one pesticide also confers low levels of resistance or tolerance to another pesticide class with a different biochemical mode of action. pathotype – A classification of a pathogen that is distinguished from others within a given species based on its pathogenicity to specific host(s). pathovar (pv.) – A subspecies or group of strains within a bacterial species that can only infect plants within a particular species, e.g., Pseudomonase syringae pv. tomato. pathosystem – A host plant species along with the parasites (bacteria, fungi, virus) that utilize the host plant. penetration resistance – Resistance associated with the selection of traits that inhibit the pesticide’s ability to reach the target site in the pest. Most commonly associated with insecticides and the selection of insects for cuticles that are less susceptible to insecticide absorbance and penetration. practical resistance – The situation where the frequency of biochemically resistant individuals in a population reaches a point at which field or commercial pesticide applications no longer provide aesthetically or economically acceptable control. This is a relative term as “acceptable levels of control” amongst crops can be variable depending on the use or value of the crop. progressive resistance – See multi-step resistance and quantitative resistance. -Q- qualitative resistance – A pattern of resistance development in populations where there is a distinct separation between sensitive and resistant individuals. Individuals are either sensitive to the pesticide or resistant to levels of the pesticide that could be feasibly used. This is typically associated with target site mutations that confer immunity to a pesticide for an individual. quantitative resistance – A pattern of resistance development in populations where there is a continuous range of sensitivity amongst individuals in a population. Individuals may have increased tolerance to a pesticide, but generally, increased doses are still be toxic. This is typically associated with target site mutations, metabolic resistance mechanisms or other genetic changes that confer tolerance but not immunity to a pesticide. -R- reduced sensitivity – Over time the population develops the ability to overcome the pesticide used and the population present evolves strains that no longer are susceptible/sensitive to an appropriate rate of pesticide. reduced uptake – The fungicide is absorbed at a much slower rate by the resistant fungus than the susceptible type (wild-type). removal – A fungal cell exports the fungicide rapidly before the chemical reaches the target site of action. resistance – Decreased sensitivity of a pest to a pesticide that results in immunity or tolerance to the pesticide; resistance must be a heritable trait with a genetic basis. resistance risk – Likelihood of resistance developing to a pesticide or within a pest population. resistance ratio – The ratio of resistant individuals relative to sensitive (wild-type) individuals in a population. This may also refer to the difference between mean population sensitivities (typically expressed as 50% effective dose (ED50) values) when populations exhibit a quantitative pattern of resistance development. resurgence – The situation where the application of a pesticide to a population containing resistance to the pesticide causes an increase in this pest’s damage or activity. This may be due to the negative affect of the pesticide on other competing pests or organisms but essentially no effect on the resistant individuals, putting them at an ecological advantage. Resurgence is also used in situations where the pesticide has not been used for awhile in an effort to revert the pathogen population to sensitive individuals. -S- single-step resistance – Resistance conferred by a single mechanism of resistance such as a single target site mutation or single metabolic change. This may also be referred to as “monogenic” resistance. See also qualitative resistance. site-specific mode-of-action – See mode of action. strain – A variant of a particular organism. sustained susceptibility – The situation where either a pest has failed to develop resistance to a pesticide despite repeated use due to biological or behavioral reasons, or a situation where biochemically resistant individuals are present but are maintained at a low level, thus practical resistance never develops. -T- target site of action – The physical site of interaction between a pesticide and the pest. For single site of action pesticides, this is a specific enzyme, protein, or molecule involved in a key biological process. For example, QoIs bind specifically to the Qo-site of cytochrome bc1. See also mode of action, which describes the biological process inhibited by the pesticide. tolerance – Reduced sensitivity of an individual pest to a pesticide conferred by genetic changes relative to a wild-type individual. Tolerant individuals may be affected by higher doses of the pesticide. -V- variant – A different genotype present within a population, such as a genotype adapted to be resistant to a pesticide. -W- wild-type population – The genotypes in a population before exposure to a pesticide or another change in the environment that results in adaptation in the pathogen. >>>>>Potential New Members and Recruiting A list of 10 new members from the discipline of plant pathology was developed and a plan discussed in an effort to increase plant pathology involvement. >>>>>Draft Webinar Development The main goal is to cover resistance terminology across the three disciplines (weed science, entomology and plant pathology). EPA staff had voiced a need for understanding and harmonization of definitions of resistance terminology across the disciplines. There is need to determine what other goals EPA has for the webinar to ensure we meet their needs. Audience for the webinar was discussed. EPA staff is the main audience. APHIS staff and legislators are also important to target. A key to success of the webinar will be working with people in each of our societies who have formal connections in DC including with EPA. >>>>>State Specific Accomplishments **Colorado Herbicide Resistant Kochia in Colorado Todd Gaines, Eric Westra, Scott Nissen, and Philip Westra Department of Bioagricultural Sciences and Pest Management Colorado State University As herbicides continue to be an essential tool for weed control, ongoing herbicide sustainability is essential in Colorado cropping systems. Research projects pertaining to the evolution and management of resistance in important species including kochia, Palmer amaranth, waterhemp, giant ragweed, and barnyardgrass are ongoing in the CSU weed science program. Several Colorado kochia samples collected in 2011 showed glyphosate resistance when tested in glyphosate dose response studies in the CSU weed science greenhouse. Some individual plants survived up to 1.25 gallons of glyphosate, although the general level of increased resistance appears to be in the 3-6 fold range. Glyphosate-resistant kochia in Colorado contains extra copies of the gene EPSPS, which encodes the protein inhibited by glyphosate. The resistant plants produce enough extra enzyme to survive normal glyphosate applications. Glyphosate-resistant kochia sampled from Colorado usually has from 4 to 10 extra copies of the EPSPS gene. We have sampled glyphosate-resistant kochia from other states and Canada, and some samples are more resistant and have 15 or more copies of the EPSPS gene. This indicates that higher resistance levels can be selected if diversity is not incorporated into kochia management programs. The CSU weed science program is conducting surveys to understand the distribution of glyphosate-resistant kochia in CO and numerous studies to look for other herbicides that can be used to control this resistant kochia. We have conducted surveys to test for glyphosate and dicamba resistance in kochia from eastern CO in 2011, 2012, and 2013. In 2011, 10% of kochia samples were classified as glyphosate resistant (defined as when >20% of tested individuals from a sample are deemed resistant). In 2012, 24% of kochia samples were classified as glyphosate resistant, and in 2013, 12% of kochia samples were glyphosate resistant. For dicamba, 11% of samples in 2012 and 9% of samples in 2013 were classified as dicamba resistant. For both glyphosate and dicamba, the samples usually contain both resistant and susceptible individuals. Importantly, some samples were resistant to both glyphosate and dicamba. Both dicamba and glyphosate are important tools for weed management in no-till and reduced tillage cropping systems. The occurrence of glyphosate-resistant and dicamba-resistant kochia populations highlights the need to incorporate diversity into weed management practices, and to take efforts to remove surviving individuals from fallow fields before they can set seed and potentially spread resistance. **Michigan Mark Whalon Maintained and updated the Arthropod Pesticide Resistance Database http://www.pesticideresistance.com/ Focused attention on the Maximum Residue Limit (MRL) issues, critical to Upper Midwest tree fruit and small fruit export/import agreements. ** South Carolina Mike Marshall Documented resistance to multiple herbicides in two weed species. Palmer amaranth (group 9, group 2 and group 3 herbicides). Italian ryegrass (group 1 and group 2 herbicides).

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