Incidence of multiple herbicide resistance in annual bluegrass (Poa annua) across southeastern Australia

Weed Science ◽  
2020 ◽  
Vol 68 (4) ◽  
pp. 340-347
Author(s):  
Rajesh Barua ◽  
Peter Boutsalis ◽  
Jenna Malone ◽  
Gurjeet Gill ◽  
Christopher Preston

AbstractAnnual bluegrass (Poa annua L.) is a problematic annual weed in established turf where the intensive use of herbicides has resulted in the evolution of herbicide resistance. In 2017, 31 populations of P. annua suspected to be resistant to herbicides commonly used to control this weed in turf were collected from golf courses across southeastern Australia to check the resistance status to different herbicide groups. All populations were found to be resistant to multiple turf herbicides. Dose–response experiments confirmed resistance to propyzamide, simazine, rimsulfuron, foramsulfuron, endothall, and pinoxaden. Levels of resistance to rimsulfuron (>56-fold), foramsulfuron (>19-fold), endothall (>7-fold), and pinoxaden (>4.3-fold) compared with the susceptible population were high, but levels of resistance to propyzamide (>2-fold) and simazine (>2-fold) were lower. Considerable variation in resistance to endothall and pinoxaden was observed among the populations of P. annua. Target-site resistance was confirmed for acetolactate synthase and acetyl-CoA carboxylase inhibitors, but not for photosystem II and microtubule assembly inhibitors. This study documented the extensive resistance to herbicides in P. annua from turf in Australia. Three of the populations investigated exhibited multiple resistance to herbicides from five mechanisms of action. The identification of multiple-resistant P. annua on several golf courses is a serious concern for turf managers.

2020 ◽  
Author(s):  
Vijay Singh ◽  
Fabricia C Reis ◽  
Casey Reynolds ◽  
Matthew Elmore ◽  
Muthukumar Bagavathiannan

Weed Science ◽  
2013 ◽  
Vol 61 (1) ◽  
pp. 21-25 ◽  
Author(s):  
J. Scott McElroy ◽  
Michael L. Flessner ◽  
Zhuoyu Wang ◽  
Fenny Dane ◽  
Robert H. Walker ◽  
...  

Annual bluegrass is commonly controlled by acetolactate synthase (ALS)-inhibiting herbicides in managed turfgrass. An annual bluegrass population with suspected resistance to ALS-inhibiting herbicides was collected from Grand National Golf Course in Opelika, AL (GN population). Subsequent testing confirmed resistance of the GN population to foramsulfuron, trifloxysulfuron, bispyribac-sodium (bispyribac), and imazaquin when compared to a susceptible population collected locally at Auburn University (AU population). Sequencing of the ALS gene revealed a point mutation resulting in an amino acid substitution at Trp574. Cloning of the ALS gene surrounding the Trp574 region yielded two distinct ALS gene sequences: one producing Trp574 and one producing Leu574. Trp574 to Leu has been previously correlated with resistance to ALS-inhibiting herbicides. Both AU and GN gene sequences contained other similar silent and missense mutations. This research confirms resistance of annual bluegrass to ALS-inhibiting herbicides with Trp574 to Leu amino acid substitution being the most likely mode of resistance based on past literature.


Weed Science ◽  
2015 ◽  
Vol 63 (1) ◽  
pp. 321-328 ◽  
Author(s):  
James T. Brosnan ◽  
Gregory K. Breeden ◽  
Jose J. Vargas ◽  
Logan Grier

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−1only controlled R annual bluegrass ≤ 40%. Similarly, simazine at 140 to 9,000 g ai ha−1only 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−1were 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.


2017 ◽  
Vol 31 (4) ◽  
pp. 609-616 ◽  
Author(s):  
James T. Brosnan ◽  
Jose J. Vargas ◽  
Eric H. Reasor ◽  
Roberto Viggiani ◽  
Gregory K. Breeden ◽  
...  

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.


2017 ◽  
Vol 31 (3) ◽  
pp. 470-476 ◽  
Author(s):  
James T. Brosnan ◽  
Jose J. Vargas ◽  
Gregory K. Breeden ◽  
Sarah L. Boggess ◽  
Margaret A. Staton ◽  
...  

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.


Weed Science ◽  
2015 ◽  
Vol 63 (SP1) ◽  
pp. 91-115 ◽  
Author(s):  
Christophe Délye ◽  
Arnaud Duhoux ◽  
Fanny Pernin ◽  
Chance W. Riggins ◽  
Patrick J. Tranel

Resistance to herbicides occurs in weeds as the result of evolutionary adaptation (Jasieniuk et al. 1996). Basically, two types of mechanisms are involved in resistance (Beckie and Tardif 2012; Délye 2013). Target-site resistance (TSR) is caused by changes in the tridimensional structure of the herbicide target protein that decrease herbicide binding, or by increased activity (e.g., due to increased expression or increased intrinsic activity) of the target protein. Nontarget-site resistance (NTSR) is endowed by any mechanism not belonging to TSR, e.g., reduction in herbicide uptake or translocation in the plant, or enhanced herbicide detoxification (reviewed in Délye 2013; Yuan et al. 2007).


Weed Science ◽  
2019 ◽  
pp. 1-6
Author(s):  
Zhaofeng Huang ◽  
Xinxin Zhou ◽  
Chaoxian Zhang ◽  
Cuilan Jiang ◽  
Hongjuan Huang ◽  
...  

Abstract Common lambsquarters (Chenopodium album L.) is one of the most troublesome weeds in soybean [Glycine max (L.) Merr.] and corn (Zea mays L.) fields in northeast China. In 2017, a C. album population that survived imazethapyr at the recommended field rate was collected from a soybean field in Heilongjiang Province in China. Experiments were conducted to determine the basis of resistance to imazethapyr and investigate the herbicide-resistance pattern in C. album. Dose–response tests showed that the resistant population (R) displayed high resistance to imazethapyr (20-fold) compared with the susceptible population (S). An in vitro acetolactate synthase (ALS) activity assay indicated that the ALS of the R population was resistant to imazethapyr compared with the ALS of the S population. Sequence analysis of the ALS gene revealed that the GCA was replaced by ACA at amino acid position 122, which resulted in an alanine to threonine substitution (Ala-122-Thr) in the R population. The R population displayed cross-resistance to thifensulfuron-methyl and flumetsulam but susceptibility to bispyribac-sodium, flucarbazone, glyphosate, mesotrione, and fomesafen. These results confirmed that the basis of imazethapyr resistance in C. album was conferred by the Ala-122-Thr substitution in the ALS enzyme. This is the first report of the target-site basis of ALS-inhibiting herbicide resistance in C. album.


Agronomy ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 874
Author(s):  
Marta Stankiewicz-Kosyl ◽  
Agnieszka Synowiec ◽  
Małgorzata Haliniarz ◽  
Anna Wenda-Piesik ◽  
Krzysztof Domaradzki ◽  
...  

Corn poppy (Papaver rhoeas L.) and cornflower (Centaurea cyanus L.) are two overwintering weed species found in crop fields in Europe. They are characterised by a similar life cycle, similar competitive efforts, and a spectrum of herbicides recommended for their control. This review summarises the biology and herbicide resistance phenomena of corn poppy and cornflower in Europe. Corn poppy is one of the most dangerous dicotyledonous weeds, having developed herbicide resistance to acetolactate synthase inhibitors and growth regulators, especially in Mediterranean countries and Great Britain. Target site resistance to acetolactate synthase inhibitors dominates among herbicide-resistant poppy biotypes. The importance of non-target site resistance to acetolactate synthase inhibitors in this species may be underestimated because non-target site resistance is very often associated with target site resistance. Cornflower, meanwhile, is increasingly rare in European agricultural landscapes, with acetolactate synthase inhibitors-resistant biotypes only listed in Poland. However, the mechanisms of cornflower herbicide resistance are not well recognised. Currently, herbicides mainly from acetolactate synthase and photosystem II inhibitors as well as from synthetic auxins groups are recommended for the control of both weeds. Integrated methods of management of both weeds, especially herbicide-resistant biotypes, continue to be underrepresented.


2012 ◽  
Vol 26 (3) ◽  
pp. 391-398 ◽  
Author(s):  
Peter Boutsalis ◽  
Gurjeet S. Gill ◽  
Christopher Preston

Herbicide resistance in rigid ryegrass is an escalating problem in grain-cropping fields of southeastern Australia due to increased reliance on herbicides as the main method for weed control. Weed surveys were conducted between 1998 and 2009 to identify the extent of herbicide-resistant rigid ryegrass across this region to dinitroaniline, and acetolactate synthase- and acetyl coenzyme A (CoA) carboxylase-inhibiting herbicides. Rigid ryegrass was collected from cropped fields chosen at random. Outdoor pot studies were conducted during the normal winter growing season for rigid ryegrass with PRE-applied trifluralin and POST-applied diclofop-methyl, chlorsulfuron, tralkoxydim, pinoxaden, and clethodim. Herbicide resistance to trifluralin in rigid ryegrass was identified in one-third of the fields surveyed from South Australia, whereas less than 5% of fields in Victoria exhibited resistance. In contrast, resistance to chlorsulfuron was detected in at least half of the cropped fields across southeastern Australia. Resistance to the cereal-selective aryloxyphenoxypropionate-inhibiting herbicides diclofop-methyl, tralkoxydim, and pinoxaden ranged between 30 and 60% in most regions, whereas in marginal cropping areas less than 12% of fields exhibited resistance. Resistance to clethodim varied between 0 and 61%. Higher levels of resistance to clethodim were identified in the more intensively cropped, higher-rainfall districts where pulse and canola crops are common. These weed surveys demonstrated that a high incidence of resistance to most tested herbicides was present in rigid ryegrass from cropped fields in southeastern Australia, which presents a major challenge for crop producers.


Weed Science ◽  
2014 ◽  
Vol 62 (1) ◽  
pp. 138-144 ◽  
Author(s):  
James T. Brosnan ◽  
Eric H. Reasor ◽  
Jose J. Vargas ◽  
Gregory K. Breeden ◽  
Dean A. Kopsell ◽  
...  

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−1was 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.I50values for the PR and SS biotypes were 0.04 and 2.8 × 10−6mM 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−1only 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−1controlled 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.


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