The Sierra Madre Sparrow Xenospiza baileyi is an endangered Mexican endemic and a bunchgrassland specialist with a disjunct range: a relatively larger population in the south-eastern Trans-Mexican Volcanic Belt, and a smaller and poorly studied population in the Sierra Madre Occidental. In the latter, known distribution and abundance consists of four localities with a maximum of 28 individuals recorded in one of them. We surveyed the Sierra Madre Sparrow in 30 sites with suitable habitat, meadows or “bajíos” with bunchgrasses, in the municipalities of Durango, Pueblo Nuevo, San Dimas, and Canatlán in the Sierra Madre Occidental of Durango. We detected a total of 193 individuals in nine (30%) of the sites (392 ha), conducting intensive searches throughout them. Bunchgrasses in confirmed meadows were composed mainly of Muhlenbergia macroura, M. rigida, M. speciosa, M. rigens, and Piptochaetium fimbriatum. Total bunchgrass area within a meadow was a significant positive predictor of the Sierra Madre Sparrow presence, while total meadow area was not a significant predictor of its abundance. Seven of the confirmed localities were previously unknown, and two of them harboured 55% of the observed individuals: Ex Hacienda Coyotes (Pueblo Nuevo) and La Lobera (San Dimas). The estimated population size is at least four times higher than any previous record (28) or suggested (40–50) for the Sierra Madre Occidental and raises an opportunity and a challenge for conserving this genetically distinct population of the Sierra Madre Sparrow in the region.

Negative interactions between guanacos Lama guanicoe and ranchers have recently intensified in central Chile because guanacos are perceived to be competing with livestock for pasture resources. We examined this conservation conflict with a novel approach that considers ranchers' subjective theories, to better understand the origins of the conflict and to identify effective conservation measures based on the participants' explanations. Our findings indicate that ranchers see the source of the current problem in a shift towards increasingly arid conditions associated with climate change. We suggest the ranchers’ perceived problems are not only caused by interspecific resource competition arising from this climatic shift, but also by reported difficulties in negotiating with governmental institutions. This study adds to knowledge of human–wildlife interactions by exploring a further dimension of the complex ecological and social interactions taking place on livestock farms. We recommend identifying effective, acceptable solutions by considering and understanding the everyday knowledge of the conflict's protagonists and their potential for change.

Prodiamine is a dinitroaniline herbicide labeled for PRE control of goosegrass in warm- and cool-season turfgrass. In 2013, several golf course roughs in Maryville, TN reported poor goosegrass control (< 20%) following prodiamine treatment at 1,120 g ai ha-1. We harvested suspected prodiamine-resistant (PR) and prodiamine-susceptible (S) goosegrass phenotypes from the field and exposed them to a range of increasing prodiamine concentrations in hydroponic culture. Exposure to prodiamine at 0.001 mM reduced root growth of the S phenotype to 11% of the non-treated check. By comparison, exposure to 0.001 mM prodiamine had minimal effect on the PR phenotype, as root growth was 94% of the non-treated check. Molecular analyses revealed that PR plants contained a threonine (Thr) to isoleucine (Ile) substitution at position 239 on the α-tubulin 1 (TUA1) protein. The substitution, found in all PR plants, is the mechanism of prodiamine resistance in this phenotype. In field studies, topramezone controlled PR goosegrass 72% to 89% by 50 d after treatment (DAT) compared to only 22% to 23% for foramsulfuron. Topramezone treatment injured bermudagrass 34% to 60% from 7 to 14 DAT; however, injury was≤6% 28 DAT and 0% by the end of the study. Our results indicate that POST applications of topramezone can control dinitroaniline-resistant goosegrass. In addition, we established an easy-to-use genotyping assay to quickly screen goosegrass phenotypes for a target-site mutation (Thr-239-Ile) on TUA1 associated with resistance to dinitroaniline herbicides such as prodiamine. Future research should work to expand this assay for use with other weed species and herbicidal modes of action.

Turfgrass managers currently have few readily available means of evaluating herbicide resistance in annual bluegrass during the growing season. Research was conducted to determine if agar-based diagnostic tests developed for agronomic weeds could be used to reliably confirm herbicide resistance in annual bluegrass harvested from golf course turf. Annual bluegrass phenotypes with target-site resistance to acetolactate synthase (ALS; R3, R7), enolpyruvylshikimate-3-phosphate synthase (EPSPS; R5), and photosystem II (PSII; R3, R4) inhibiting herbicides were included in experiments along with an herbicidal susceptible phenotype (S). Single tiller plants were washed free of soil and transplanted into autoclavable polycarbonate plant culture boxes filled with plant tissue culture agar amended with a murashigee-skoog medium and trifloxysulfuron (6.25, 12.5, 25, 50, 75, 100, or 150 μM), glyphosate (0, 6, 12, 25, 50, 100, 200, or 400 μM), or simazine (0, 6, 12, 25, 50, 100, 200, or 400 μM). Mortality in agar was assessed 7 to 10 days after treatment (depending on herbicide) and compared to responses observed after treating individual plants of each phenotype with trifloxysulfuron (28 g ai ha-1), glyphosate (1120 g ae ha-1), or simazine (1120 g ai ha-1) in an enclosed spray chamber. Fisher’s exact test (α = 0.05) determined that mortality in agar with 12.5 μM trifloxysulfuron and 100 μM glyphosate was not significantly different than treating whole plants via traditional spray application. Mortality with all concentrations of simazine in agar was significantly different than that observed after treating resistant and susceptible phenotypes via traditional spray application. Our findings indicate that an agar-based diagnostic assay can be used to detect annual bluegrass resistance to ALS- or EPSPS-inhibiting herbicides in less than 10 days; however, additional research is needed to refine this assay for use with PSII-inhibiting herbicides.

Methiozolin is an isoxazoline herbicide being investigated for selective POST annual bluegrass control in managed turfgrass. Research was conducted to evaluate methiozolin efficacy for controlling two annual bluegrass phenotypes with target-site resistance to photosystem II (PSII) or enolpyruvylshikimate-3-phosphate synthase (EPSPS)-inhibiting herbicides (i.e., glyphosate), as well as phenotypes with multiple resistance to microtubule and EPSPS or PSII and acetolactate synthase (ALS)-inhibiting herbicides. All resistant phenotypes were established in glasshouse culture along with a known herbicide-susceptible control and treated with methiozolin at 0, 125, 250, 500, 1000, 2000, 4000, or 8000 g ai ha−1. Methiozolin effectively controlled annual bluegrass with target-site resistance to inhibitors of EPSPS, PSII, as well as multiple resistance to EPSPS and microtubule inhibitors. Methiozolin rates required to reduce aboveground biomass of these resistant phenotypes 50% (GR50 values) were not significantly different from the susceptible control, ranging from 159 to 421 g ha−1. A phenotype with target-site resistance to PSII and ALS inhibitors was less sensitive to methiozolin (GR50=862 g ha−1) than a susceptible phenotype (GR50=423 g ha−1). Our findings indicate that methiozolin is an effective option for controlling select annual bluegrass phenotypes with target-site resistance to several herbicides.

The herbicide pinoxaden is a phenylpyrazoline inhibitor of acetyl coenzyme A carboxylase. Research was conducted to determine the effects of pinoxaden (90 g ai ha−1) alone and in combination with herbicide safeners on creeping bentgrass injury as well as perennial ryegrass and roughstalk bluegrass control. Greenhouse experiments determined that herbicide safeners cloquintocet-mexyl, fenchlorazole-ethyl, and mefenpyr-diethyl were more effective in reducing creeping bentgrass injury from pinoxaden than benoxacor, isoxadifen-ethyl, and naphthalic-anhydride. Other experiments determined that creeping bentgrass injury from pinoxaden decreased as rates (0, 23, 45, 68, 90, 225, or 450 g ha−1) of cloquintocet-mexyl, fenchlorazole-ethyl, and mefenpyr-diethyl increased. On the basis of creeping bentgrass responses to various safener rates, safeners were applied at 68 and 450 g ha−1 in additional experiments to evaluate their effects on pinoxaden (90 g ha−1) injury to creeping bentgrass and efficacy against perennial ryegrass and roughstalk bluegrass. In these experiments, safeners mefenpyr-diethyl and cloquintocet-mexyl reduced pinoxaden-induced creeping bentgrass injury (from 25 to ≤ 5%) more than fenchlorazole-ethyl at 2 wk after treatment. Safeners reduced pinoxaden efficacy against roughstalk bluegrass. Perennial ryegrass was controlled > 80% by pinoxaden and herbicide safeners did not reduce control. Field experiments should evaluate pinoxaden in combination with cloquintocet-mexyl and mefenpyr-diethyl to optimize safener : herbicide ratios and rates for creeping bentgrass safety as well as perennial ryegrass and roughtstalk bluegrass control in different climates and seasons.

Research studies evaluated effects of the auxin transport inhibitor, diflufenzopyr, on the biokinetics and efficacy of aminocyclopyrachlor-methyl ester (AMCP-ME) applications to black nightshade and large crabgrass. Absorption, translocation, and metabolism of 14C-AMCP-ME was quantified with and without diflufenzopyr (35 g ai ha−1). Diflufenzopyr had minimal effects on translocation of radioactivity in either species. Accumulation of radioactivity in aboveground plant sections of black nightshade was greater than or equal to that in large crabgrass by 72 h after treatment (HAT). In both species, metabolism of 14C-AMCP-ME was rapid, as 60 to 78% of the extracted radioactivity was the free acid metabolite 8 HAT. In the greenhouse, black nightshade and large crabgrass were treated with AMCP-ME (9, 18, and 35 g ai ha−1) alone and in combination with diflufenzopyr (35 g ha−1). Mixtures of AMCP-ME plus diflufenzopyr did not increase large crabgrass control compared with AMCP-ME alone at any time. Diflufenzopyr (35 g ha−1) increased black nightshade control with AMCP-ME (18 and 35 g ha−1) 7 d after treatment (DAT). However, this increase in control was not observed 14 or 28 DAT. All treatments containing AMCP-ME controlled large crabgrass 70 to 79% 28 DAT compared with > 93% for black nightshade at the same time point.

Annual bluegrass resistance to inhibitors of acetolactate synthase (ALS) and photosystem II (PSII) in managed turf has been confirmed in the southeastern United States. A biotype of annual bluegrass that had developed resistance (R) to the PSII inhibitor simazine was not controlled by POST applications of foramsulfuron or trifloxysulfuron in 2011 or 2012. In whole plant dose-response experiments, trifloxysulfuron, simazine, and indaziflam controlled a susceptible (S) population of annual bluegrass > 91% when applied POST to nontillering plants. However, trifloxysulfuron applications at 3.5 to 223 g ai ha−1 only controlled R annual bluegrass ≤ 40%. Similarly, simazine at 140 to 9,000 g ai ha−1 only controlled R annual bluegrass ≤ 20%. R annual bluegrass plants were more tolerant to indaziflam applied POST to leaf stage plants prior to tillering, as rates > 100 g ai ha−1 were needed to control R annual bluegrass ≥ 96%. No differences in the activity of ALS in R and S plants exposed to increasing foramsulfuron concentrations from 0 to 100 µM were detected suggesting that nontarget mechanisms could explain reduced efficacy of POST herbicide applications in whole plant dose-response experiments. Applications of indaziflam (35 to 70 g ha−1) and oxadiazon (2,240 to 4,500 g ai ha−1) effectively controlled R annual bluegrass when applied PRE. This biotype of R annual bluegrass is the first reported instance of a weed developing resistance to multiple modes of action in managed turf. Education is needed among turf managers regarding the consequences of exclusive use of the same herbicides for annual bluegrass control leading to the onset of herbicide resistance.

Research was conducted to determine the efficacy of aminocyclopyrachlor in comparison to glyphosate, clopyralid, fluroxypyr, and triclopyr for silk tree (commonly known as mimosa) control. In the greenhouse, aminocyclopyrachlor was applied at 8.75, 17.5, 35, and 70 g ha−1 with and without methylated seed oil (MSO) at 0.5% v/v. Efficacy of these treatments was compared to glyphosate and triclopyr at 1,350 g ha−1, fluroxypyr at 103 g ha−1, and clopyralid at 100 g ha−1. Few differences in silk tree control were detected by 28 d after treatment (DAT), as aminocyclopyrachlor with MSO controlled silk tree 87 to 100% compared to 53 to 100% for aminocyclopyrachlor without MSO. Aminocyclopyrachlor at 35 g ha−1 provided silk tree control similar to glyphosate, triclopyr, clopyralid, and fluroxypyr regardless of adjuvant. Inclusion of MSO enhanced initial activity of aminocyclopyrachlor after application. At 7 DAT, 8.75 g ha−1 of aminocyclopyrachlor plus MSO controlled silk tree similar to aminocyclopyrachlor alone at 70 g ha−1. In laboratory studies, absorption of 14C-aminocyclopyrachlor 2 h after treatment (HAT) with MSO measured 93% compared to only 62% for 14C-aminocyclopyrachlor without MSO. By 24 HAT, absorption of 14C-aminocyclopyrachlor measured 99 and 71% for applications with and without MSO, respectively. Increased foliar absorption with MSO may explain enhanced activity observed 7 DAT in greenhouse studies, as no effects in 14C-aminocyclopyrachlor translocation due to adjuvant were observed. Responses suggest MSO increased the speed of silk tree control with aminocyclopyrachlor and may also improve rainfastness of aminocyclopyrachlor applications for control of silk tree and other woody species.

Glasshouse research was conducted to investigate the efficacy of herbicide safeners for improving creeping bentgrass (CBG) tolerance to various herbicides. CBG injury from amicarbazone (150 g ha−1), bispyribac-sodium (110 g ha−1), fenoxaprop-p-ethyl (35 g ha−1), imazapic (45 g ha−1), quinclorac (1,050 g ha−1), or topramezone (37 g ha−1) applied in combination with the herbicide safeners naphthalic anhydride or isoxadifen-ethyl was evaluated. These safeners reduced CBG injury from topramezone only. Topramezone was then applied in combination with naphthalic anhydride, isoxadifen-ethyl, cloquintocet-mexyl (cloquintocet), fenchlorazole-ethyl, mefenpyr-diethyl, and benoxacor. These experiments determined that CBG injury was lowest from topramezone in combination with cloquintocet. Additional experiments evaluated topramezone (37 g ha−1) with several rates of cloquintocet and determined that applications at ≥ 28 g ha−1 reduced CBG injury similarly. Cloquintocet (28 g ha−1) increased topramezone I50 values against CBG, but not large crabgrass or goosegrass. The cytochrome P450 (cP450) inhibitor malathion (1000 g ha−1) reduced topramezone I50 values against CBG in one experimental run. Topramezone–cloquintocet combinations warrant further research in field settings.

Mesotrione, a 4-hydroxyphenylpyruvate dioxygenase-inhibiting herbicide, is labeled for PRE and POST crabgrass control. It has enhanced efficacy on smooth and large crabgrass when applied in conjunction with soil-applied nitrogen (N). The objectives of this study, using crabgrass as the weed species, were to (1) determine the influence of N rate and tissue N concentration on mesotrione activity, (2) determine the influence of N source on mesotrione activity, and (3) determine the influence of N application timing on mesotrione activity. Large crabgrass plants that received 12 kg N ha−1 or more before mesotrione application had more bleached and necrotic leaves compared with plants that received 0 kg N ha−1 7 d after treatment (DAT) in the greenhouse. Although N application rates as high as 98 kg N ha−1 were tested, 90% leaf bleaching and necrosis were observed with rates of 8.9 or 10.1 kg N ha−1 in Tennessee and Indiana, respectively. Nitrogen concentration in large crabgrass leaf and stem tissue on the day of the mesotrione application was closely related to the bleaching and necrosis symptoms observed 7 DAT. Although N rate influenced mesotrione activity, N source did not. Nitrogen application timing was also important, with N applications 3, 1, and 0 d before a mesotrione application having the highest percentage of bleached and necrotic leaves in greenhouse experiments. Both greenhouse and field trials support the finding that N applications in proximity to the mesotrione application enhance herbicide activity. Thus, practitioners can pair N and POST mesotrione applications together or in proximity to enhance crabgrass control.

Prodiamine is a mitotic inhibiting herbicide regularly used to control annual bluegrass PRE. A population of annual bluegrass not controlled by prodiamine at 1,120 g a.i. ha−1 was identified on a golf course in Alcoa, TN, in 2012. A whole-plant hydroponics bioassay was used to screen this biotype for prodiamine resistance (PR) compared with a known susceptible population (SS). Multitiller (i.e., > 4 tillers) PR and SS annual bluegrass plants were established in hydroponic culture and exposed to 0, 0.001, 0.01, 0.10, 1.0, and 10.0 mM prodiamine. Exposure to prodiamine at 0.001 mM reduced root growth of the SS biotype to 26% of the nontreated check (i.e., 0 mM prodiamine) but had no effect on the PR biotype. When exposed to 10 mM prodiamine, root growth of the PR biotype was reduced to 24% of the nontreated check compared with 9% for the SS biotype. I50 values for the PR and SS biotypes were 0.04 and 2.8 × 10−6 mM prodiamine, respectively. The PR biotype measured lower in plant height and leaf width than the SS population. In field trials, prodiamine at 560, 840, 1,120, and 1,400 g ha−1 only controlled the PR biotype 0 to 22%. PRE applications of the cellulose biosynthesis inhibitor indaziflam at 35, 52.5, and 70 g a.i. ha−1 controlled this PR biotype 70 to 97%. This marks the second instance of annual bluegrass developing resistance to prodiamine in Tennessee during the past 5 yr. Future research should evaluate indaziflam efficacy for control of other prodiamine-resistant biotypes of annual bluegrass as well as annual bluegrass biotypes resistant to herbicidal inhibitors of 5-enolpyruvylshikimic acid-3-phosphate synthase, acetolactate synthase, and photosystem II.