Absorption, translocation, and metabolism of AC 263,222 by leafy spurge were studied over 8 d. Based on the amount of herbicide applied and recovered from the leaf surfaces, 40% of applied AC 263,222 was absorbed by leafy spurge 2 d after treatment (DAT), with no further absorption observed by 8 DAT. Eight DAT, 19% of applied [14C]-AC 263,222 had translocated to below-ground plant parts while 4% was exuded from the roots into the sand media. AC 263,222 was not metabolized 2 DAT in the crown, root, and root buds, but 42% was metabolized in the treated leaves. Only 17% of recovered [14C] was AC 263,222 in treated leaves 8 DAT (83% metabolized), while AC 263,222 accounted for 70% of recovered [14C] in the root and root buds. HPLC analysis indicated that the balance of [14C] was associated with a single, polar metabolite. Total recovery of [14C] was 88% at 8 DAT.

To broaden the spectrum of herbicides useful in potato production, the bxn gene for bromoxynil resistance, which encodes a nitrilase specific for bromoxynil, was introduced into ‘Lemhi Russet’ potato by Agrobacterium tumefaciens-mediated transformation. In GR50 studies, transformed potato clones were at least 70-fold more resistant to bromoxynil than the untransformed control. Resistance was due to rapid metabolism of bromoxynil to 3,5-dibromo-4-hydroxybenzoic acid, followed by conjugation to polar compounds. In yield trials, the best performing transgenic clones had total tuber yields equal to the untreated, untransformed control, but U.S. No. 1 tuber yields were 15 to 30% lower than the untreated, untransformed control. Tubers from three out of four transgenic clones had specific gravities, percent solids, and fry color similar to or better than the untreated, untransformed control. The data suggest that lower U.S. No. 1 yields in the transgenic clones were due to somaclonal variation and that expression of the bxn transgene had no consistent, detrimental effect on internal tuber quality.

Imazamox-resistant hybrids resulted from a cross between jointed goatgrass and an imazamox-resistant wheat (cv. FS-4 IR wheat). Two imazamox-resistant hybrids were discovered in a research plot where FS-4 IR wheat seed had been replanted from the harvest of an imazamox efficacy study conducted the year before at a different location. These hybrid plants survived imazamox applied at 0.053 and 0.069 kg ai ha−1 in the field and produced seven viable seeds (BC1). This seed germinated, and chromosomes were counted from the roots (2N number ranged from 39 to 54). In the greenhouse, six of the seven plants survived an application of 0.072 kg ai ha−1imazamox, which confirmed that the resistance trait had been passed to these progeny. A large amount of phenotypic variation was observed in the mature BC1 plants. A genetic description of the movement of the resistant gene is proposed based on the case of the gene being located on the D and the A or B genomes. Management strategies to reduce the occurrence of herbicide-resistant hybrids are presented.

A false cleavers population that survived treatment with triasulfuron/bromoxynil in 1996 was identified in central Alberta, Canada, in a field that had been treated with acetolactate synthase (ALS) inhibitors in 3 of the previous 6 yr. In greenhouse studies, this biotype was highly resistant to the ALS inhibitors triasulfuron, thifensulfuron/tribenuron, and sulfometuron and moderately resistant to imazethapyr; GR50, values were > 16, > 5, > 1.0, and 9.9, respectively. In addition, cross-resistance was identified to the auxin-type herbicide quinclorac (GR50 value > 6.7) but not to fluroxypyr (GR50 value 1) or MCPA/mecoprop/dicamba. Quinclorac had not been used previously in this field. Analysis of ALS extracted from the resistant biotype and a susceptible biotype from a nearby location indicated that resistance to ALS inhibitors was due to an altered target site with reduced sensitivity to a broad range of ALS inhibitors. The ALS I50 values for triasulfuron, metsulfuron, chlorsulfuron, thifensulfuron, and imazethapyr were 36, 34, 92, 96, and 14 times higher, respectively, for the resistant compared to the susceptible biotype. The mechanism of resistance to quinclorac is unknown. This is the first report of high-level herbicide resistance in this weed species.

Tank-mixed combinations of pyridate and 2,4-DB were synergistic with respect to sicklepod control and independent with respect to Florida beggarweed control and peanut tolerance in greenhouse studies. Leaf absorption of 14C-pyridate was generally enhanced by the addition of 2,4-DB. Translocation of 14C-pyridate out of the treated leaf did exceed 21% of the amount absorbed across all species, and 14C-pyridate was not affected by the addition of 2,4-DB. Sensitivity of peanut, Florida beggarweed, and sicklepod to pyridate was independent of both adsorption and translocation. Metabolic detoxification of pyridate into a benign metabolite was highest in the tolerant peanut, lowest in highly susceptible Florida beggarweed, and intermediate in slightly susceptible sicklepod. Absorption of 14C-2,4-DB by peanut was increased by approximately 10% with the addition of pyridate. No such increase was observed in either Florida beggarweed or sicklepod. Translocation of 14C-2,4-DB out of the treated leaf was not affected by the addition of pyridate in any of the three species evaluated.

Laboratory studies were conducted to determine the effect of SAN 582 on the absorption, translocation, and metabolism of sethoxydim in johnsongrass and soybean. 14C-sethoxydim absorption in johnsongrass and soybean was enhanced 4 h after application when tank mixed with SAN 582. Absorption in johnsongrass increased from 18% with 14C-sethoxydim applied alone to 65% when applied with SAN 582. Absorption in soybean increased from 30% with 14C-sethoxydim applied alone to 83% when applied with SAN 582. The addition of crop oil concentrate also enhanced foliar absorption of 14C-sethoxydim. Eight hours after application, foliar absorption in johnsongrass increased from 22% with 14C-sethoxydim applied alone to 61% when 14C-sethoxydim was applied with crop oil concentrate. Foliar absorption in soybean increased from 38% with 14C-sethoxydim applied alone to 59% when 14C-sethoxydim was applied with crop oil concentrate. When 14C-sethoxydim was applied in combination with crop oil concentrate and SAN 582, foliar absorption was 84% or more in both johnsongrass and soybean 4 h after application and did not increase over time. Minor differences in translocation were observed, but these differences were not sufficient to account for the increase in foliar activity observed when SAN 582 is tank mixed with sethoxydim. SAN 582 did not affect metabolism of sethoxydim in either species. Based on these data, it appears that SAN 582 increases the efficacy of sethoxydim by enhancing foliar absorption.

Black nightshade was subjected to two degrees of water stress by adding polyethylene glycol 20,000 (PEG) to the nutrient solution 5 d before treatment with glyphosate. The ED50 values for glyphosate, determined from dose-response curves, demonstrated that both degrees of water stress strongly increased the ED50, with and without the surfactant Ethomeen T/25 in the spray solution. The surfactant reduced the ED50 5-, 4.6-, and 6.9-fold at 0, 15, and 20% PEG, respectively. A 14C study demonstrated that unstressed plants absorbed 22% of applied glyphosate. Without surfactant, water stress reduced foliar absorption 2.2-fold at 15% PEG and 4.5-fold at 20% PEG. With surfactant, the foliar absorption was 35% of the applied amount in unstressed and water-stressed plants. The surfactant and PEG reduced the translocation efficiency of glyphosate. The surfactant had the most pronounced influence and reduced the translocation efficiency 1.5-fold at 0% PEG, 2.2-fold at 15% PEG, and 1.8-fold at 20% PEG. Induction or removal of water stress 24 h after glyphosate treatment indicated that plant growth rate is positively correlated with glyphosate efficacy. It was concluded that the surfactant can overcome the adverse influence of water stress on foliar absorption of glyphosate but not the adverse, postapplication influence of water stress on glyphosate efficacy.

A common waterhemp biotype that was not controlled by triazine or acetolactate synthase (ALS)-inhibiting herbicides was isolated from a field in Bond County, IL, in the fall of 1996. Greenhouse and laboratory experiments determined resistance to atrazine and three ALS-inhibiting herbicides in this biotype. Based on whole-plant response, the Bond County common waterhemp biotype required over 1,000 times more imazethapyr relative to a susceptible biotype to reduce growth 50%. Cross-resistance to thifensulfuron, a sulfonylurea, and flumetsulam, a triazolopyrimidine sulfonanilide, was also detected. Based on in vivo enzyme assays, ALS in the Bond County common waterhemp biotype was 20-, > 8-, and 68-fold less sensitive than ALS in the susceptible biotype to imazethapyr, thifensulfuron, and flumetsulam, respectively. Whole-plant efficacy trials also indicated that the Bond County common waterhemp biotype required more than 20 kg ha−1 of atrazine to inhibit growth 50%. Chlorophyll fluorescence assays revealed that 100 nM atrazine inhibited photosynthesis in the susceptible biotype, whereas 10 M did not affect photosynthesis in the resistant biotype. Regions of the genes encoding ALS and D1 proteins were sequenced to determine the molecular basis for the resistances. Triazine resistance was conferred by a glycine for serine substitution at residue 264 of the D1 protein, while ALS resistance was conferred by a leucine for tryptophan substitution at residue 569 of ALS.

A shattercane biotype resistant to primisulfuron was identified during greenhouse evaluations of seed obtained from southeastern and south-central Nebraska fields previously treated with primisulfuron or nicosulfuron a minimum of 3 consecutive yr. Absorption, translocation, metabolism, and acetolactate synthase (ALS) assay experiments were conducted to determine resistance mechanism(s) by comparing ALS-susceptible forage sorghum (ROX) to resistant shattercane (RS). The ROX had 10 and 12% greater 14C absorption than RS 24 and 96 hours after treatment (HAT), respectively. Absorption of 14C increased over time for both ROX and RS, while 14C translocation from the treated leaf to the shoots and roots was similar for ROX and RS. Unmetabolized primisulfuron accounted for > 80% of the radioactivity recovered 24 h after application for both ROX and RS. The ROX and RS had similar ALS-specific activities and total protein concentrations. Km values for RS and ROX were 10.4 and 5.8 mM pyruvate, respectively. The ALS isolated from RS was less sensitive than ROX to inhibition by primisulfuron. The I50 values for RS and ROX were 231 and 0.025 μM primisulfuron, respectively. The mechanism of primisulfuron resistance in this RS biotype is an altered ALS with decreased sensitivity to primisulfuron.

In vitro acetolactate synthase (ALS) activity from three commercial imidazolinone-resistant corn hybrids (ICI 8692 IT, Pioneer 3751 IR, and Ciba 4393 IMR) was compared to imidazolinone-sensitive isogenic hybrid controls for sensitivity to 11 herbicides representing four classes of ALS-inhibiting herbicide chemistry. Acetolactate synthase activity from Pioneer IR and Ciba IMR was cross-resistant to all four classes of ALS inhibitors, ranging from 48- to 5,000-fold. The ICI IT hybrid displayed only four- to eightfold resistance to the six imidazolinone herbicides and the pyrimidinylthiobenzoate herbicide, pyrithiobac, but no cross-resistance to the sulfonylurea and triazolopyrimidine sulfonanilide herbicides. The four- to eightfold enzyme resistance to imidazolinone herbicides provides whole-plant resistance; however, the sevenfold enzyme resistance to pyrithiobac was insufficient to afford whole-plant protection to a field application rate of the herbicide. A second imidazolinone-specific resistance allele, XI-12, currently under commercial development, was examined for the level of dominance at the enzyme level. In the heterozygous state, imazethapyr resistance was fivefold, compared to 250-fold in the homozygous condition, indicating XI-12 is a semidominant trait. No cross-resistance to nicosulfuron or primisulfuron was observed in the heterozygous XI-12 hybrid extracts nor to nicosulfuron in the XI-12 homozygote; however, a fivefold resistance to primisulfuron was detected in the XI-12 homozygote.

Greenhouse, laboratory, and field studies were conducted to evaluate the potential of nonionic surfactant (NIS), crop oil concentrate (COC), methylated seed oil (MSO), and 28% urea ammonium nitrate (UAN) to enhance whole plant efficacy, absorption, and spray retention of foliar applications of isoxaflutole to giant foxtail. In greenhouse studies, isoxaflutole at 10 g ai ha−1 reduced giant foxtail growth 5%, whereas the addition of a spray adjuvant reduced giant foxtail growth at least 75%. The addition of UAN improved giant foxtail growth reduction when used in combination with isoxaflutole plus NIS. Isoxaflutole spray retention on the leaf surface was increased with an adjuvant and a further increase was observed with the addition of UAN. Isoxaflutole applied with NIS, COC, and MSO resulted in 42, 60, and 91% 14C absorption, respectively, compared to 21% absorption from isoxaflutole applied alone 24 h after treatment (HAT). Increased 14C absorption and entry into the cuticle when an adjuvant was utilized with isoxaflutole resulted in greater translocation of 14C from isoxaflutole out of the treated leaf. Significant basipetal movement from foliar applications of 14C-isoxaflutole suggests phloem mobility. In field studies, isoxaflutole applied with MSO provided greater giant foxtail growth reduction compared to isoxaflutole applied with NIS and in some cases COC. The addition of UAN to isoxaflutole did not increase whole plant efficacy in field studies. These studies indicate isoxaflutole has excellent potential to be used for control of existing giant foxtail present at the time of corn planting if an adequate adjuvant is utilized.

This symposium is a first in the history of our society. We have never before devoted a portion of the annual meeting to formal consideration of the ethical aspects of our work. It is significant to me that after 38 annual meetings, 42 years of existence, and 45 volumes of our journal, we have begun to discuss the ethics of weed science. I applaud the vision of the Board of Directors that provided funding to bring two of our speakers to the meeting. The Board has always provided capable management of the society's affairs. By management, I mean that we have been well organized to proceed in the direction we are headed. Voting to hold this symposium and providing funding is, in my view, an act of leadership, by which I mean, thinking about moving in a new direction, in a direction not dictated by the past. When disciplines proactively begin to examine the ethical dimensions of their science and technology, society may begin to believe that scientists recognize and act upon their social responsibilities. This would be a welcome and refreshing development in these days when public distrust and disillusionment with science may be as high as they have ever been (Lockwood 1997).

The noxious weed yellow starthistle is commonly controlled by the auxinic herbicide picloram. Induction of ethylene synthesis, epinasty, and reduction in shoot growth are typical symptoms of picloram treatment. Picloram did not induce ethylene evolution in the resistant accession RDW-1, though it caused a 250% increase in ethylene evolution in the susceptible wildtype SCI-1. The ethylene synthesis inhibitor aminoethoxyvinylglycine reduced the amount of ethylene induced by picloram in SCI-1 to control levels, but only reduced epinasty by 20% after 6 d. Aminoethoxyvinylglycine did not affect the reduction in shoot weight caused by picloram. The ethylene-releasing compound ethephon induced only a small amount of epinasty and had little effect on shoot weight in either accession. These results suggest that ethylene induced by picloram in wildrype plants plays only a minor role in the herbicidal effects of picloram. Furthermore, the resistance of the RDW-1 accession is not due to the lack of ethylene biosynthesis following picloram application to this accession.

Inbreeding coefficients were determined for nine southeastern Idaho kochia populations using chlorsulfuron resistance as a phenotypic marker. Inbreeding coefficients in six of the populations approximated 0, indicating that these field populations were random mating. One population had an inbreeding coefficient of 0.32, indicating partial selfing. No susceptible genotypes were identified in one population, which suggested recent selection and skewed the inbreeding coefficient. One population had an inbreeding coefficient of −0.19, suggesting either heterozygote advantage or some recent selection in the population. Our results suggest that kochia populations generally approximate random mating. Therefore, unlinked alleles will be independently assorted in field populations of kochia.