Artykuły w czasopismach na temat „ALS inhibitor resistance”
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Beckie, Hugh J., Suzanne I. Warwick i Connie A. Sauder. "Basis for Herbicide Resistance in Canadian Populations of Wild Oat (Avena fatua)". Weed Science 60, nr 1 (marzec 2012): 10–18. http://dx.doi.org/10.1614/ws-d-11-00110.1.
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Wild oat is the second-most abundant, but most economically important, weed across the Canadian Prairies of western Canada. Despite the serious economic effects of resistance to acetyl-CoA carboxylase (ACC) or acetolactate synthase (ALS) inhibitors or both in this weed throughout the Northern Great Plains of North America, little research has examined the basis for herbicide resistance. We investigated target-site and nontarget-site mechanisms conferring ACC- and ALS-inhibitor resistance in 16 wild oat populations from across western Canada (four ACC-inhibitor resistant, four ALS-inhibitor resistant, and eight ACC- and ALS-inhibitor resistant). TheACC1mutations were found in 8 of the 12 ACC inhibitor-resistant populations. The Ile1781Leu mutation was detected in three populations, the Trp2027Cys and Asp2078Gly mutations were in two populations each, and the Trp1999Cys, Ile2041Asn, Cys2088Arg, and Gly2096Ser substitutions were in one population each. Three populations had twoACC1mutations. Only 2 of the 12 ALS inhibitor-resistant populations had anALStarget-site mutation—Ser653Thr and Ser653Asn substitutions. This is the first global report ofALStarget-site mutations inAvenaspp. and four previously undocumentedACC1mutations in wild oat. Based on these molecular analyses, seedlings of five ACC + ALS inhibitor-resistant populations (one with anACC1mutation; four with noACCorALSmutations) were treated with malathion, a known cytochrome P450 monooxygenase inhibitor, followed by application of one of four ACC- or ALS-inhibiting herbicides. Malathion treatment often resulted in control or suppression of these populations, suggesting involvement of this enzyme system in contributing to resistance to both ACC and ALS inhibitors.
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Eberlein, Charlotte V., Mary J. Guttieri, Philip H. Berger, John K. Fellman, Carol A. Mallory-Smith, Donn C. Thill, Roger J. Baerg i William R. Belknap. "Physiological consequences of mutation for ALS-inhibitor resistance". Weed Science 47, nr 4 (sierpień 1999): 383–92. http://dx.doi.org/10.1017/s0043174500091967.
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Biochemical and physiological effects of target site resistance to herbicides inhibiting acetolactate synthase (ALS) were evaluated using sulfonylurea-resistant (R) and -susceptible (S) near isonuclearLactuca sativa‘Bibb’ lines derived by backcrossing the resistance allele fromLactuca serriolaL. intoL. sativa.Sequence data suggest that resistance inL. sativais conferred by a single-point mutation that encodes a proline197to histidine substitution in Domain A of the ALS protein; this is the same substitution observed in RL. serriola. Kmapp(pyruvate) values for ALS isolated from R and SL. sativawere 7.3 and 11.1 mM, respectively, suggesting that the resistance allele did not alter the pyruvate binding domain on the ALS enzyme. Both R and S ALS had greater affinity for 2-oxobutyrate than for pyruvate at the second substrate site. Ratios of acetohydroxybutyrate: acetolactate produced by R ALS across a range of 2-oxobutyrate concentrations were similar to acetohydroxybutyrate: acetolactate ratios produced by S ALS. Specific activity of ALS from RL. sativawas 46% of the specific activity from SL. sativa, suggesting that the resistance allele has detrimental effects on enzyme function, expression, or stability. ALS activity from R plants was less sensitive to feedback inhibition by valine, leucine, and isoleucine than ALS from S plants. Valine, leucine, and isoleucine concentrations were about 1.5 times higher in R seed than in S seed on a per gram of seed basis, and concentrations of valine and leucine were 1.3 and 1.6 times higher, respectively, in R leaves than in S leaves. Findings suggest that the mutation for resistance results in altered regulation of branched-chain amino acid synthesis.
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Guo, Jiaqi, Chance W. Riggins, Nicholas E. Hausman, Aaron G. Hager, Dean E. Riechers, Adam S. Davis i Patrick J. Tranel. "Nontarget-Site Resistance to ALS Inhibitors in Waterhemp (Amaranthus tuberculatus)". Weed Science 63, nr 2 (czerwiec 2015): 399–407. http://dx.doi.org/10.1614/ws-d-14-00139.1.
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A waterhemp population (MCR) previously characterized as resistant to 4-hydroxyphenylpyruvate dioxygenase and photosystem II inhibitors demonstrated both moderate and high levels of resistance to acetolactate synthase (ALS) inhibitors. Plants from the MCR population exhibiting high resistance to ALS inhibitors contained the commonly found Trp574Leu ALS amino acid substitution, whereas plants with only moderate resistance did not have this substitution. A subpopulation (JG11) was derived from the MCR population in which the moderate-resistance trait was isolated from the Trp574Leu mutation. Results from DNA sequencing and ALS enzyme assays demonstrated that resistance to ALS inhibitors in the JG11 population was not due to an altered site of action. This nontarget-site ALS-inhibitor resistance was characterized with whole-plant dose–response experiments using herbicides from each of the five commercialized families of ALS-inhibiting herbicides. Resistance ratios ranging from 3 to 90 were obtained from the seven herbicides evaluated. Nontarget-site resistance to ALS has been rarely documented in eudicot weeds, and adds to the growing list of resistance traits evolved in waterhemp.
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Beckie, Hugh J., Linda M. Hall, Scott Meers, James J. Laslo i F. Craig Stevenson. "Management Practices Influencing Herbicide Resistance in Wild Oat". Weed Technology 18, nr 3 (wrzesień 2004): 853–59. http://dx.doi.org/10.1614/wt-03-124r.
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A 3-yr study was conducted in Wheatland County, Alberta to determine if agronomic practices of growers influenced the occurrence of herbicide resistance in wild oat. Wild oat seeds were collected in 33 fields in 1997 and in 31 fields in each of 1998 and 1999 (one field per grower). Seedlings were screened for resistance to two acetyl-CoA carboxylase (ACCase) inhibitors, imazamethabenz, an acetolactate synthase (ALS) inhibitor, and triallate, a thiocarbamate herbicide. A questionnaire on herbicide resistance awareness and management practices was completed by each grower. Both ACCase and ALS inhibitor resistance in wild oat were linked to a lack of crop rotation diversity. In addition, ALS inhibitor–resistant wild oat was associated with conservation-tillage systems and recent use of herbicides with that mode of action. Results of this study suggest that timely tillage and inclusion of fall-seeded and perennial forage crops in rotations will effectively slow the selection of resistance in this grass species.
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Varanasi, Vijay K., Jason K. Norsworthy, Chad Brabham i Robert C. Scott. "Characterization of Acetolactate Synthase (ALS)-Inhibitor Resistance in Pennsylvania smartweed (Persicaria pensylvanica)". Weed Science 66, nr 6 (21.09.2018): 710–14. http://dx.doi.org/10.1017/wsc.2018.44.
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AbstractPennsylvania smartweed [Persicaria pensylvanica(L.) M. Gómez] is a common weed of rice (Oryza sativaL.) in the midsouthern United States and has recently become a concern for farmers because of reduced tillage systems. Acetolactate synthase (ALS) inhibitors have been extensively used for controlling smartweeds in imidazolinone-resistant and conventional rice. In the present study, we confirmed resistance to commonly used ALS inhibitors in rice and characterized the underlying resistance mechanism in aP. pensylvanicabiotype from southeast Missouri. A dose–response experiment was conducted in the greenhouse using bensulfuron-methyl, imazethapyr, and bispyribac-sodium to determine the resistance index (resistance/susceptibility [R/S]) based on GR50estimates. The target-siteALSgene was amplified from R and S plants, and sequences were analyzed for mutations known to confer ALS-inhibitor resistance. TheP. pensylvanicabiotype in question was found to be resistant to bensulfuron-methyl (R/S=2,330), imazethapyr (R/S=12), and bispyribac-sodium (R/S=6). Sequencing of theALSgene from R plants revealed two previously known mutations (Pro-197-Ser, Ala-122-Ser) conferring resistance to sulfonylureas and imidazolinones. This is the first report of ALS-inhibitor resistance inP. pensylvanica.
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Beckie, H. J., L. M. Hall, F. J. Tardif i G. Séguin-Swartz. "Acetolactate synthase inhibitor-resistant stinkweed (Thlaspi arvense L.) in Alberta". Canadian Journal of Plant Science 87, nr 4 (1.10.2007): 965–72. http://dx.doi.org/10.4141/cjps06019.
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Two stinkweed populations from southern and central Alberta were not controlled by acetolactate synthase (ALS)-inhibiting herbicides in 2000. This study reports on their cross-resistance to ALS-inhibiting herbicides, molecular basis of resistance, and inheritance of resistance. Both putative herbicide-resistant biotypes responded similarly to increasing doses of the herbicides. The biotypes were highly resistant to ethametsulfuron and exhibited a low level of resistance to metsulfuron and imazethapyr. However, both biotypes were not resistant to florasulam, a triazolopyrimidine ALS inhibitor, or sulfometuron, a non-selective sulfonylurea ALS inhibitor. The cross-resistance pattern was consistent with the confirmed target-site mutation. Sequence analysis of the ALS gene detected a Pro197Leu mutation in both biotypes. Similar to many other ALS inhibitor-resistant weed biotypes, resistance was conferred by a single dominant gene. This study confirms the first global occurrence of herbicide resistance in this species. Key words: ALS-inhibitor resistance, ALS sequence, herbicide resistance, target-site mutation
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Tranel, Patrick J., Chenxi Wu i Ahmed Sadeque. "Target-Site Resistances to ALS and PPO Inhibitors Are Linked in Waterhemp (Amaranthus tuberculatus)". Weed Science 65, nr 1 (13.12.2016): 4–8. http://dx.doi.org/10.1614/ws-d-16-00090.1.
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It is generally expected that, in the case of multiple herbicide resistance, different resistance mechanisms within a weed will follow Mendel’s law of independent assortment. Research was conducted to investigate anecdotal observations suggesting that target site–based resistances to inhibitors of acetolactate synthase (ALS) and protoporphyrinogen oxidase (PPO) did not follow independent assortment in common waterhemp. Cosegregation of the two resistances was observed in backcross lines (population sensitive to both herbicides as recurrent parent). Specifically, whereas 52% of backcross plants were resistant to a PPO inhibitor, this percentage increased to 92% when the backcross plants were preselected for resistance to an ALS inhibitor. Molecular marker analysis confirmed that the corresponding genes (ALSandPPX2) were genetically linked. When data from all plants analyzed were pooled, the genetic distance between the two genes was calculated to be 7.5 cM. The two genes were found to be about 195 kb apart in the recently published grain amaranth genome, explaining the observed genetic linkage. There is likely enough recombination that occurs between the linked genes to prevent the linkage from having significant implications in terms of resistance evolution. Nevertheless, documentation of the happenstance linkage between target-site genes for resistance to ALS and PPO inhibitors in waterhemp is a reminder that one should not assume distinct resistance mechanism will independently assort.
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Beckie, Hugh J., i Xavier Reboud. "Selecting for Weed Resistance: Herbicide Rotation and Mixture". Weed Technology 23, nr 3 (wrzesień 2009): 363–70. http://dx.doi.org/10.1614/wt-09-008.1.
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Herbicide rotations and mixtures are widely recommended to manage herbicide resistance. However, little research has quantified how these practices actually affect the selection of herbicide resistance in weeds. A 4-yr experiment was conducted in western Canada from 2004 to 2007 to examine the impact of herbicide rotation and mixture in selecting for acetolactate synthase (ALS) inhibitor resistance in the annual broadleaf weed, field pennycress, co-occurring in wheat. Treatments consisted of the ALS-inhibitor herbicide, ethametsulfuron, applied in a mixture with bromoxynil/MCPA formulated herbicide (photosystem-II inhibitor/synthetic auxin), or in rotation with the non-ALS inhibitor at an ALS-inhibitor application frequency of 0, 25, 50, 75, and 100% (i.e., zero to four applications, respectively) over the 4-yr period. The field pennycress seed bank at the start of the experiment contained 5% ethametsulfuron-resistant seed. Although weed control was only marginally reduced, resistance frequency of progeny of survivors increased markedly after one ALS-inhibitor application. At the end of the experiment, the level of resistance in the seed bank was buffered by susceptible seed, increasing from 29% of recruited seedlings after one application to 85% after four applications of the ALS inhibitor. The level of resistance in the seed bank for the mixture treatment after 4 yr remained similar to that of the nontreated (weedy) control or 0% ALS-inhibitor rotation frequency treatment. The results of this study demonstrate how rapidly ALS-inhibitor resistance can evolve as a consequence of repeated application of herbicides with this site of action, and supports epidemiological information from farmer questionnaire surveys and modeling simulations that mixtures are more effective than rotations in mitigating resistance evolution through herbicide selection.
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Tseng, Te-Ming, Swati Shrestha, James D. McCurdy, Erin Wilson i Gourav Sharma. "Target-site Mutation and Fitness Cost of Acetolactate Synthase Inhibitor-resistant Annual Bluegrass". HortScience 54, nr 4 (kwiecień 2019): 701–5. http://dx.doi.org/10.21273/hortsci13512-18.
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Annual bluegrass (Poa annua L.) is an annual weed that is particularly troublesome in managed turfgrass. It has been controlled conventionally with herbicides, including acetolactate synthase (ALS) inhibitors. However, resistance to ALS inhibitors has been documented throughout the southeastern United States since 2012. A rate–response trial was conducted to confirm and determine the resistance level of suspected resistant P. annua biotypes from Mississippi (Reunion), followed by DNA sequencing to determine whether the mechanism of resistance is a target-site mutatio n. In addition, a fitness assay was conducted together with a susceptible biotype to determine whether resistance to ALS inhibitors is associated with decreased fitness. Reunion was at least 45 times more resistant to foramsulfuron than the standard susceptible biotype based on I50 estimates [I50 is the rate of herbicide giving a 50% response (50% visual necrosis)], requiring a predicted 331 g a.i./ha foramsulfuron for 50% control. DNA sequencing results identified a Trp574-to-Leu mutation in the ALS gene of the Reunion biotype, which has been shown by other studies to confer resistance to ALS inhibitors. Measurement of fitness parameters among the Reunion and susceptible biotypes demonstrated reduced seed yield, tillering, and flowering time in the resistant Reunion biotype, suggesting that ALS inhibitor resistance is possibly correlated to decreased fitness in P. annua. Alternative methods to control P. annua need to be considered as a result of the evolution of herbicide-resistant biotypes. An integrated management strategy to control P. annua weeds will help prevent further evolution of resistance. Because this study evaluated only the target-site mechanism of resistance, it is also necessary to determine whether the resistant biotype has reduced uptake, translocation, or enhanced metabolism as additional mechanisms of resistance. Consequently, a fitness study encompassing a more comprehensive list of plant parameters will provide conclusions of the fitness costs associated with ALS inhibitor resistance in P. annua. Chemical names: Foramsulfuron {1-(4,6-dimethoxypyrimidin-2-yl)-3-[2-(dimethylcarbamoyl)-5-formamidophenylsulfonyl] urea}.
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Molin, William T., Vijay K. Nandula, Alice A. Wright i Jason A. Bond. "Transfer and Expression of ALS Inhibitor Resistance from Palmer Amaranth (Amaranthus palmeri) to anA. spinosus×A. palmeriHybrid". Weed Science 64, nr 2 (czerwiec 2016): 240–47. http://dx.doi.org/10.1614/ws-d-15-00172.1.
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Transfer of herbicide resistance among closely related weed species is a topic of growing concern. A spiny amaranth × Palmer amaranth hybrid was confirmed resistant to several acetolactate synthase (ALS) inhibitors including imazethapyr, nicosulfuron, pyrithiobac, and trifloxysulfuron. Enzyme assays indicated that the ALS enzyme was insensitive to pyrithiobac and sequencing revealed the presence of a known resistance conferring point mutation, Trp574Leu. Alignment of the ALS gene for Palmer amaranth, spiny amaranth, and putative hybrids revealed the presence of Palmer amaranth ALS sequence in the hybrids rather than spiny amaranth ALS sequences. In addition, sequence upstream of the ALS in the hybrids matched Palmer amaranth and not spiny amaranth. The potential for transfer of ALS inhibitor resistance by hybridization has been demonstrated in the greenhouse and in field experiments. This is the first report of gene transfer for ALS inhibitor resistance documented to occur in the field without artificial/human intervention. These results highlight the need to control related species in both field and surrounding noncrop areas to avoid interspecific transfer of resistance genes.
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Pandian, Balaji Aravindhan, Abigail Friesen, Martin Laforest, Dallas E. Peterson, P. V. Vara Prasad i Mithila Jugulam. "Confirmation and Characterization of the First Case of Acetolactate Synthase (ALS)-Inhibitor—Resistant Wild Buckwheat (Polygonum convolvulus L.) in the United States". Agronomy 10, nr 10 (1.10.2020): 1496. http://dx.doi.org/10.3390/agronomy10101496.
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Wild buckwheat (Polygonum convolvulus L.) is a problem weed and ALS-inhibitors (e.g., chlorsulfuron) are commonly used for its management. Recently, a population of wild buckwheat (KSW-R) uncontrolled with ALS-inhibitors was found in a wheat field in Kansas, USA. The objectives of this research were to determine the level and mechanism of resistance to chlorsulfuron and cross resistance to other ALS-inhibitors in the KSW-R population. In response to chlorsulfuron rates ranging from 0 to 16x (x = 18 g ai/ha), the KSW-R wild buckwheat was found >100-fold more resistant compared to a known ALS-inhibitor susceptible (KSW-S) wild buckwheat. Also, >90% of KSW-R plants survived field recommended rates of sulfonylurea but not imidazolinone family of ALS-inhibitors. A portion of the ALS gene covering all previously reported mutations known to bestow resistance to ALS-inhibitors was sequenced from both KSW-R and KSW-S plants. The Pro-197-Ser substitution that confers resistance to the sulfonylurea herbicides was found in KSW-R plants. Our results support the evolution of high level of chlorsulfuron resistance as a result of a mutation in the ALS-gene in KSW-R buckwheat. This is the first case of resistance to any herbicides in wild buckwheat in the US.
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Ashigh, Jamshid, i François J. Tardif. "ALS-Inhibitor Resistance in Populations of Eastern Black Nightshade (Solanum ptycanthum) from Ontario". Weed Technology 20, nr 2 (czerwiec 2006): 308–14. http://dx.doi.org/10.1614/wt-05-034r.1.
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Populations of eastern black nightshade suspected of being resistant to acetolactate synthase (ALS) inhibitors have been reported since 1999 in different locations in Ontario, Canada. This event has threatened the use of ALS inhibitors for control of this species. The objectives of this study were to evaluate the spectrum of resistance to different ALS-inhibiting herbicides and to examine the effectiveness of alternative modes of action herbicides. Growth room experiments were conducted to determine the response to imazethapyr and atrazine in seven suspected ALS inhibitor– resistant populations. One resistant and one susceptible population were further characterized for their response to ALS inhibitors and chloroacetamides. Seven populations were able to survive imazethapyr at 100 g ai/ha, while there was no resistance to atrazine. Compared to a susceptible (S) population, resistant (R) population SOLPT 1 had 726-, 31-, 6-, and 4-fold resistance to postemergence (POST) applied imazethapyr, imazamox, primisulfuron, and flumetsulam, respectively. Preemergence (PRE) application of imazethapyr, flumetsulam, cloransulam, nicosulfuron, prosulfuron, and rimsulfuron did not provide control of the R population, whereas they totally controlled the S population. The chloroacetamide herbicides metolachlor, dimethenamid, and flufenacet all provided at least 90% control of both R and S populations when applied PRE at the recommended field rates. The ALS inhibitors will not provide adequate control of these resistant populations, but acceptable control could be achieved with chloroacetamides or with atrazine.
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Patzoldt, William L., i Patrick J. Tranel. "Multiple ALS Mutations Confer Herbicide Resistance in Waterhemp (Amaranthus tuberculatus)". Weed Science 55, nr 5 (październik 2007): 421–28. http://dx.doi.org/10.1614/ws-06-213.1.
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In a survey of herbicide responses among Illinois waterhemp half-sib populations, several were observed with differential responses to imazethapyr and thifensulfuron, two acetolactate synthase (ALS)–inhibiting herbicides. Plants from two waterhemp populations were verified resistant to imazethapyr, but susceptible to chlorimuron, using a nondestructive leaf-disc assay. Sequencing of the ALS gene revealed that imazethapyr-resistant waterhemp plants from both populations had inferred amino acid substitutions at position 653 of ALS. Depending on the population, the serine at position 653 of ALS was substituted with either asparagine (S653N) or threonine (S653T). Waterhemp lines were derived from each population to create uniformly imidazolinone-resistant (IR) waterhemp biotypes, designated IR-62 and IR-101. ALS-inhibitor responses of each IR biotype were compared with a previously identified ALS inhibitor–resistant biotype with a tryptophan to leucine substitution at position 574 (W574L) and an herbicide-susceptible control. Whole-plant dose–response experiments with waterhemp biotypes containing W574L, S653N, or S653T mutations indicated that each biotype was resistant to imazethapyr, but only the biotype with a W574L mutation was resistant to thifensulfuron. In vitro ALS-activity assays revealed unique patterns of cross-resistance among protein extracts derived from each biotype in response to imazethapyr, thifensulfuron, cloransulam, and pyrithiobac. In conclusion, three different forms of target-site–based resistance to ALS inhibitors have been identified in waterhemp.
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Hinz, John R. R., i Micheal D. K. Owen. "Acetolactate Synthase Resistance in a Common Waterhemp (Amaranthus rudis) Population". Weed Technology 11, nr 1 (marzec 1997): 13–18. http://dx.doi.org/10.1017/s0890037x00041269.
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Research was initiated to determine (a) whether a common waterhemp population was resistant to acetolactate synthase (ALS) inhibiting herbicides, (b) the percentage of the population that was ALS-inhibitor resistant, (c) the resistance mechanism, and (d) the effectiveness of a whole plant assay to detect ALS-inhibitor resistance. ALS-inhibitor resistance was confirmed in a common waterhemp population near Davis City, IA. The Davis City common waterhemp population was cross resistant to both imidazolinone and sulfonylurea herbicides, but not to lactofen. Approximately 10% of the Davis City common waterhemp population was sensitive to a rate of imazaquin 4 times the normal field rate. Davis City common waterhemp isolated ALS was much less sensitive to imazaquin and primisulfuron inhibition than was grain amaranth or an ALS-sensitive common waterhemp isolated ALS. Imazaquin I50values were 366.4 and 3.4 μM for ALS isolated from Davis City common waterhemp and grain amaranth, respectively. Primisulfuron I50values were 3.6 and 0.007 μM for ALS isolated from Davis City common waterhemp and grain amaranth, respectively. A whole plant ALS assay was developed that allowed for much more rapid detection of an ALS-resistant species and used less plant material than a conventional ALS assay.
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Christoffers, Michael J., Vijay K. Nandula, Kirk A. Howatt i Todd R. Wehking. "Target-site resistance to acetolactate synthase inhibitors in wild mustard (Sinapis arvensis)". Weed Science 54, nr 02 (kwiecień 2006): 191–97. http://dx.doi.org/10.1614/ws-05-030r.1.
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Inhibitors of acetolactate synthase (ALS) are important herbicides for control of wild mustard, a common weed of the north central United States and Canada. Wild mustard that survived treatments with the ALS inhibitors cloransulam, imazethapyr, and thifensulfuron was sampled from a North Dakota soybean field in 1999. The mechanism of resistance and response of this wild mustard biotype to ALS-inhibiting herbicides was investigated. In vitro enzyme-inhibition experiments confirmed a resistance mechanism associated with the ALS enzyme; imazethapyr or imazamox at 1 × 10−4M caused only 10 to 11% and 12 to 16% reductions in ALS activity, respectively. ALS from a susceptible wild mustard biotype was inhibited 50% (I50) with imazethapyr at 8 × 10−7M or imazamox at 1.1 × 10−6M. Whole-plant greenhouse treatments confirmed cross-resistance across ALS-inhibitor classes. Treatment with twice-normal field rates of thifensulfuron, ethametsulfuron, triflusulfuron, imazamox, imazethapyr, flumetsulam, cloransulam, flucarbazone, and imazamethabenz reduced biomass of the susceptible biotype at least 96% 28 d after treatment. Biomass of the resistant biotype was reduced 49% by triflusulfuron and 35% by thifensulfuron, but was not reduced by other herbicides. DNA sequence analysis of ALS genes from resistant and susceptible biotypes revealed a point mutation inferring a Trp-to-Leu amino acid substitution in ALS of the resistant biotype. This mutation, corresponding to position 574 of theArabidopsisALS amino acid sequence, is known to confer cross-resistance to ALS-inhibiting herbicides and is the probable cause of resistance in the wild mustard biotype. Phylogenetic analysis of wild mustard and canola ALS sequences confirmed that the Trp574mutation arose within wild mustard and was not derived via introgression from imidazolinone-resistant canola. The results of this research indicate a naturally occurring target-site point mutation responsible for conferring cross-resistance to ALS-inhibiting herbicides in this wild mustard biotype.
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Werle, Rodrigo, Kevin Begcy, Melinda K. Yerka, Jeffrey P. Mower, Ismail Dweikat, Amit J. Jhala i John L. Lindquist. "Independent Evolution of Acetolactate Synthase–inhibiting Herbicide Resistance in WeedySorghumPopulations across Common Geographic Regions". Weed Science 65, nr 1 (styczeń 2017): 164–76. http://dx.doi.org/10.1614/ws-d-16-00095.1.
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Traditional breeding has been used to develop grain sorghum germplasm that is tolerant to acetolactate synthase (ALS)-inhibiting herbicides (Inzen Technology, DuPont). Inzen sorghum carries a double mutation in the ALS gene (Val560Ile and Trp574Leu), which confers high level of tolerance to ALS-inhibiting herbicides. Overreliance on ALS-inhibiting herbicides for weed control during the 1990s resulted in the evolution of ALS inhibitor–resistant shattercane populations in Nebraska. According to a survey conducted in 2013, ALS inhibitor–resistant weedySorghumpopulations persist in Nebraska. The objectives of this research were to determine whether the ALS mutations present in Inzen sorghum were present in the ALS inhibitor–resistant shattercane and johnsongrass populations detected in Nebraska and northern Kansas, and whether these populations evolved ALS resistance independently. Primers specific to the Val560and Trp574region of the ALS gene were used to screen the populations with PCR. The Trp574Leu mutation was present in one ALS inhibitor–resistant johnsongrass population. The Val560Ile was detected in three ALS inhibitor–resistant shattercane, one susceptible shattercane, one ALS inhibitor–resistant johnsongrass, and one susceptible johnsongrass population. Moreover, Val560Ile was present in resistant and/or susceptible individuals within johnsongrass and shattercane populations that were segregating for ALS resistance, indicating that by itself the Val560Ile mutation does not confer resistance to ALS-inhibiting herbicides. None of the populations presented both mutations simultaneously, as does Inzen sorghum. A shattercane population containing the Ser653Thr mutation was also detected. This research indicates that the ALS mutations present in Inzen sorghum already exist individually in weedy sorghum populations. Moreover, our results present strong evidence that ALS resistance in these populations evolved independently. Thus, widespread overreliance on ALS-inhibiting herbicides prior to adoption of glyphosate-tolerant crops in the 1990s exerted sufficient selective pressure on shattercane and johnsongrass populations for resistance to evolve multiple times in the Midwest. Finally, a survey of the 5′ portion of the ALS gene in more diverse wild and weedySorghumspecies was hampered by limited coverage in genomic resequencing surveys, suggesting that refined PCR-based methods will be needed to assess SNP variation in this gene region, which includes the Ala122, Pro197, and Ala205codons known to confer ALS resistance in other species.
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Kumar, Vipan, Prashant Jha, Darci Giacomini, Eric P. Westra i Philip Westra. "Molecular Basis of Evolved Resistance to Glyphosate and Acetolactate Synthase-Inhibitor Herbicides in Kochia (Kochia scoparia) Accessions from Montana". Weed Science 63, nr 4 (grudzień 2015): 758–69. http://dx.doi.org/10.1614/ws-d-15-00021.1.
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The rapid evolution and spread of glyphosate-resistant (GR) kochia in the Northern Great Plains is an increasing threat to GR cropping systems and conservation tillage practices common in this region. GR kochia accessions with 4.6- to 11-fold levels of resistance to glyphosate have recently been reported in Montana. Those GR kochia accessions were also suspected to be resistant to acetolactate synthase (ALS) inhibitors, i.e., multiple herbicide-resistant (MHR) kochia. In this research, the level of resistance to the ALS-inhibitor herbicides (sulfonylureas) and the molecular mechanisms conferring resistance to glyphosate and ALS-inhibitor herbicides in MHR kochia was investigated. On the basis of whole-plant dose–response assays, MHR kochia accessions (GIL01, JOP01, and CHES01) were 9.3- to 30-fold more resistant to premixed thifensulfuron methyl + tribenuron methyl + metsulfuron methyl than the susceptible (SUS) accession. In an in vivo leaf-disk shikimate assay, MHR plants accumulated less shikimate than the SUS plants at a discriminate dose of 100 μM glyphosate. Sequencing of the conserved region ofEPSPSrevealed no target-site mutation at Thr102or Pro106residue. MHR kochia accessions had increased relativeEPSPSgene copies (~ 4 to 10) compared with the SUS accession (single copy). Furthermore, MHR kochia accumulated higher EPSPS protein compared with the SUS plants. Resistance to the ALS-inhibitor herbicides was conferred by Pro197amino acid substitution (proline to glutamine).EPSPSgene amplification and a single target-site mutation at Pro197inALSgene confer resistance to glyphosate and ALS-inhibitor herbicides, respectively, in MHR kochia accessions from Montana. This is the first confirmation of occurrence of MHR kochia in Montana.
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Liu, Jian, Jiapeng Fang, Zongzhe He, Jun Li i Liyao Dong. "Target site–based resistance to penoxsulam in late watergrass (Echinochloa phyllopogon) from China". Weed Science 67, nr 4 (20.05.2019): 380–88. http://dx.doi.org/10.1017/wsc.2019.14.
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AbstractLate watergrass [Echinochloa phyllopogon (Stapf) Koso-Pol.] is one of the most persistent weeds in rice fields and shows resistance to some acetolactate synthase (ALS)-inhibiting herbicides, such as penoxsulam. Previous studies of E. phyllopogon’s herbicide resistance have focused on non–target site resistance mechanisms. In this study, E. phyllopogon populations from Heilong Jiang Province, China, that were possibly resistant to penoxsulam were used to identify the target site–based mechanisms of resistance. Population HSRH-520 showed a 25.4-fold higher resistance to penoxsulam than the sensitive population, HSRH-538. HSRH-520 was resistant to other ALS inhibitors, with resistance indexes ranging from 17.1 to 166. Target-gene sequence analysis revealed two different ALS genes in E. phyllopogon; a Pro-197-Ser substitution occurred in the ALS-2 gene of HSRH-520. In vitro activity assays revealed that the penoxsulam concentrations required to inhibit 50% of the ALS activity were 13.7 times higher in HSRH-520 than in HSRH-538. Molecular-docking tests showed that the Pro-197-Ser mutation reduced the binding affinity between ALS and ALS inhibitors belonging to the triazolopyrimidine, sulfonylaminocarbonyltriazolinone, and sulfonylurea families, and there were almost no effects on binding affinity when the ALS inhibitors were of the pyrimidinylthiobenzoate and imidazolinone families. Overall, the results indicated and verified that the Pro-197-Ser mutation leads to increased ALS activity by reducing the binding affinity of the inhibitor and ALS. This is the first report on the Pro-197-Ser mutation in the complete ALS gene of E. phyllopogon and will aid future research of target site–based resistance mechanisms of E. phyllopogon to ALS inhibitors.
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Shergill, Lovreet S., Jenna Malone, Peter Boutsalis, Christopher Preston i Gurjeet Gill. "Basis of ACCase and ALS inhibitor resistance inHordeum glaucumSteud". Pest Management Science 73, nr 8 (15.02.2017): 1638–47. http://dx.doi.org/10.1002/ps.4501.
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Osuna, M. D., i R. De Prado. "Conyza albida : a new biotype with ALS inhibitor resistance". Weed Research 43, nr 3 (9.05.2003): 221–26. http://dx.doi.org/10.1046/j.1365-3180.2003.00337.x.
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Beckie, Hugh J., Suzanne I. Warwick i Connie A. Sauder. "Acetolactate Synthase (ALS) Inhibitor-Resistant Wild Buckwheat (Polygonum convolvulus) in Alberta". Weed Technology 26, nr 1 (marzec 2012): 156–60. http://dx.doi.org/10.1614/wt-d-11-00096.1.
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Wild buckwheat is the most abundant broadleaf weed across the Prairie region of western Canada. Acetolactate synthase (ALS)-inhibiting herbicides are commonly used to control this species and other broadleaf weeds in cereal crops. A field survey in Alberta in 2007 identified a single population that was putatively resistant to ALS-inhibiting herbicides. In herbicide resistance screening in the greenhouse, all F1 progeny tested were resistant to the ALS-inhibiting herbicides thifensulfuron/tribenuron, a sulfonylurea herbicide, or florasulam, a triazolopyrimidine herbicide; dose response of shoot biomass indicated the population was 10- and 20-fold less sensitive to thifensulfuron/tribenuron and florasulam, respectively, than a susceptible control population. ALS gene sequencing of 24 F1 progeny indicated that the Trp574Leu target-site mutation was responsible for conferring ALS-inhibitor resistance in this biotype, the first global report of ALS-inhibitor resistance for this species. Because this mutation typically endows high-level resistance across all five ALS-inhibitor classes, this wild buckwheat biotype may only be controlled by a different site-of-action herbicide.
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Beckie, Hugh J., Linda M. Hall, Scott W. Shirriff, Elise Martin i Julia Y. Leeson. "Glyphosate and acetolactate synthase inhibitor resistance in Russian thistle (Salsola tragus L.) in Alberta". Canadian Journal of Plant Science 99, nr 3 (1.06.2019): 384–87. http://dx.doi.org/10.1139/cjps-2018-0252.
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A survey was conducted in Alberta in 2017 to determine the distribution and abundance of acetolactate synthase (ALS) inhibitor and glyphosate resistance in Russian thistle. Of 45 populations tested, 31 (62%) were ALS inhibitor resistant. No populations exhibited resistance to glyphosate. This survey serves as a baseline to monitor future incidence of resistance in this weed.
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Takano, Hudson Kagueyama, Rubem Silvério de Oliveira Junior, Jamil Constantin, Guilherme Braga Pereira Braz, Luiz Henrique Morais Franchini i Nilda Roma Burgos. "Multiple resistance to atrazine and imazethapyr in hairy beggarticks (Bidens pilosa )". Ciência e Agrotecnologia 40, nr 5 (październik 2016): 547–54. http://dx.doi.org/10.1590/1413-70542016405022316.
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ABSTRACT Resistance to herbicides is a serious threat to crop production worldwide, especially in agronomic crops and cereals. This research evaluated the possible occurrence of Bidens pilosa resistant to imazethapyr and atrazine in Brazil. The resistant biotype was collected from an area with a history of repeated application of photosystem II (PSII) and ALS inhibitor herbicides. The susceptible biotype was collected from an area with no history of herbicide application. Resistance verification experiments were carried out in the greenhouse. The treatments were arranged in a 3 x 8 factorial scheme, where the first factor was populations [susceptible (S), parent resistant (PR), and resistant F1 (RF1)]; and the second factor was herbicide dose (0, 375, 750, 1500, 3000, 6000, 12000 and 24000 g ha-1 for atrazine; or 0, 12.5, 25, 50, 100, 200, 400 and 800 g ha-1 for imazethapyr). The resistance factor to atrazine was 2.83 for PR and 5.55 for RF1. This population was more resistant to imazethapyr (>21-fold) than it was to atrazine. The recommended maximum dose of the herbicides did not control this B. pilosa population adequately. The data support the claim that B. pilosa population from this field in Quarto Centenário, Parana is resistant to two herbicide modes of action - PSII inhibitor (i.e. atrazine) and ALS inhibitor (i.e. imazethapyr). This is the first report of such case for this species, globally. Cross-resistance to other ALS inhibitors and other PS II inhibitors as well as the respective mechanisms of resistance to each herbicide are being investigated.
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Monquero, Patrícia Andrea, Pedro Jacob Christoffoleti i Helaine Carrer. "Biology, management and biochemical/genetic characterization of weed biotypes resistant to acetolactate synthase inhibitor herbicides". Scientia Agricola 60, nr 3 (2003): 495–503. http://dx.doi.org/10.1590/s0103-90162003000300013.
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Bidens pilosa and Amaranthus quitensis are major weeds infesting soybean [Glycine max L (Merrill)] fields in Brazil and Argentina. The repetitive use of acetolactate synthase (ALS EC 4.1.3.18) inhibiting herbicides in São Gabriel do Oeste, MS, Brazil and in the provinces of Córdoba and Tucumã, Argentina, has selected for resistant (R) biotypes of these weeds. Research work was developed to study the management, growth, biochemistry, and genetics of these R weed biotypes. In a field experiment it was found that chlorimuron-ethyl and imazethapyr at recommended rates (both ALS inhibitor herbicides), did not control R B. pilosa, but the alternative lactofen, fomesafen and bentazon were effective, either sprayed alone or mixed with the ALS inhibitor herbicides. Greenhouse studies confirmed the cross-resistance of both R biotypes to the imidazolinone and sulfonylurea herbicides, and these alternative herbicides, when sprayed alone or mixed with the ALS inhibitor, efficiently controlled both R and S populations. A growth analysis of the R and S biotypes of these weeds, under non-competitive conditions, indicated that there is no adaptive cost to the R biotypes (pleiotropic effect). A quick bioassay using ALS and ketoacid reductoisomerase (KARI) inhibitors showed that the resistance of the R biotypes to herbicides is related to a lack of sensitivity of the ALS enzyme to the herbicides. On the other hand, the sequencing of the gene that codifies the ALS resistance in R A. quitensis did not present any mutation in the A Domain region, suggesting that other positions of the gene that confer insensitivity of the ALS to sulfonylurea and imidazolinone herbicides could have mutated.
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Eberlein, Charlotte V., Mary J. Guttieri, Carol A. Mallory-Smith, Donn C. Thill i Roger J. Baerg. "Altered acetolactate synthase activity in ALS-inhibitor resistant prickly lettuce (Lactuca serriola)". Weed Science 45, nr 2 (kwiecień 1997): 212–17. http://dx.doi.org/10.1017/s0043174500092730.
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The effect of target site mutation for acetolactate synthase (ALS)-inhibitor resistance on ALS activity was evaluated in a sulfonylurea-resistant (R) biotype of prickly lettuce with a proline173to histidine substitution in Domain A of the ALS enzyme. I50values for ALS inhibition by several ALS-inhibitor herbicides were determined for R and susceptible (S) biotypes. Results from both a standard ALS assay and a chloroplast assay for ALS activity showed that the R biotype also was cross-resistant to representatives of the imidazolinone (imazethapyr) and triazolopyrimidine (flumetsulam) families, but was not cross-resistant to the pyrimidinyl oxybenzoate (4,6-dimethoxypyrimidin-2-y 1-oxy-2-benzoic acid) tested. TheKm(pyruvate) was similar for ALS extracted from the R and S biotypes, suggesting that mutation for resistance did not alter pyruvate binding on the enzyme. However, specific activity of ALS from the R biotype was 57% less than specific activity of ALS from the S biotype, suggesting that the resistance mutation may affect enzyme function, expression, or stability. ALS from the R biotype was less sensitive to inhibition by the branched chain amino acids, valine, leucine, and isoleucine, than ALS from the S biotype. Reduced sensitivity to feedback inhibition was correlated with 70, 40, and 9% higher concentrations of valine, leucine, and isoleucine, respectively, on a per seed basis in R vs. S seed.
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Lamego, Fabiane P., Dirk Charlson, Carla A. Delatorre, Nilda R. Burgos i Ribas A. Vidal. "Molecular Basis of Resistance to ALS-Inhibitor Herbicides in Greater Beggarticks". Weed Science 57, nr 5 (październik 2009): 474–81. http://dx.doi.org/10.1614/ws-09-056.1.
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Soybean is a major crop cultivated in Brazil, and acetolactate synthase (ALS)-inhibiting herbicides are widely used to control weeds in this crop. The continuous use of these ALS-inhibiting herbicides has led to the evolution of herbicide-resistant weeds worldwide. Greater beggarticks is a polyploid species and one of the most troublesome weeds in soybean production since the discovery of ALS-resistant biotypes in 1996. To confirm and characterize the resistance of greater beggarticks to ALS inhibitors, whole-plant bioassays and enzyme experiments were conducted. To investigate the molecular basis of resistance in greater beggarticks theALSgene was sequenced and compared between susceptible and resistant biotypes. Our results confirmed that greater beggarticks is resistant to ALS inhibitors and also indicated it possesses at least three isoforms of theALSgene. Analysis of the nucleotide and deduced amino acid sequences among the isoforms and between the biotypes indicated that a single point mutation, G–T, in oneALSisoform from the resistant biotype resulted in an amino acid substitution, Trp574Leu. Two additional substitutions were observed, Phe116Leu and Phe149Ser, in a second isoform of the resistant biotype, which were not yet reported in any other herbicide-resistantALSgene; thus, their role in conferring herbicide resistance is not yet ascertained. This is the first report ofALSmutations in an important, herbicide-resistant weed species from Brazil.
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Li, Dan, Xiangju Li, Huilin Yu, Jingjing Wang i Hailan Cui. "Cross-Resistance of Eclipta (Eclipta prostrata) in China to ALS Inhibitors Due to a Pro-197-Ser Point Mutation". Weed Science 65, nr 5 (19.06.2017): 547–56. http://dx.doi.org/10.1017/wsc.2017.16.
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Eclipta, widespread in tropical, subtropical, and temperate regions, is one of the main malignant broadleaf weeds and thrives in moist and dryland fields. Field rates of acetolactate synthase (ALS) inhibitors have failed to control eclipta in some farmlands in China. One ALS inhibitor–resistant population (R) collected from Jiangsu province in China was confirmed in the greenhouse in our preliminary work. Whole-plant assays revealed that this R population was highly resistant to four sulfonylureas (pyrazosulfuron-ethyl, 134-fold; bensulfuron-methyl, 172-fold; metsulfuron-methyl, 30-fold; and tribenuron-methyl, 195-fold), two triazolopyrimidines (pyroxsulam, 98-fold; penoxsulam, 30-fold), and one pyrimidinylthio-benzoate (bispyribac-sodium, 166-fold) and was moderately resistant to two imidazolinones (imazethapyr, 10-fold; imazapic, 19-fold). ALS enzyme-activity assays showed insensitivity of the ALS from the R population (resistance index values ranged from 12 to 293) to all of the above ALS inhibitors in vitro. Chromatograms fromALSgene sequence analysis detected a homozygous Pro-197-Ser amino acid substitution in the R population. These results confirmed that the Pro-197-Ser substitution results in broad-spectrum cross-resistance to ALS inhibitors in the eclipta R population. To our knowledge, this study is the first to report broad cross-resistance to ALS inhibitors in eclipta and to obtain the full-lengthALSgene sequence.
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Beckie, Hugh J., Linda M. Hall, Scott W. Shirriff, Elise Martin i Julia Y. Leeson. "Triple-resistant kochia [Kochia scoparia (L.) Schrad.] in Alberta". Canadian Journal of Plant Science 99, nr 2 (1.04.2019): 281–85. http://dx.doi.org/10.1139/cjps-2018-0256.
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A randomized stratified survey was conducted in Alberta in 2017 to determine the distribution and abundance of multiple-resistant [acetolactate synthase (ALS) inhibitor, glycine, and synthetic auxin] kochia. All populations were ALS inhibitor resistant, with glyphosate and dicamba resistance confirmed in 50% and 18% of populations, respectively. Ten percent of populations exhibited resistance to all three mode-of-action herbicides.
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Varanasi, Vijay K., Chad Brabham, Nicholas E. Korres i Jason K. Norsworthy. "Nontarget site resistance in Palmer amaranth [Amaranthus palmeri(S.) Wats.] confers cross-resistance to protoporphyrinogen oxidase-inhibiting herbicides". Weed Technology 33, nr 2 (kwiecień 2019): 349–54. http://dx.doi.org/10.1017/wet.2019.12.
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AbstractPalmer amaranth is one of the most problematic weeds in cropping systems of North America, especially in midsouthern United States, because of its competitive ability and propensity to evolve resistance to several herbicide sites of action. Previously, we confirmed and characterized the first case of nontarget site resistance (NTSR) to fomesafen in a Palmer amaranth accession from Randolph County, AR (RCA). The primary basis of the present study was to evaluate the cross- and multiple-resistance profile of the RCA accession. The fomesafen dose-response assay in the presence of malathion revealed a lower level of RCA resistance when compared with fomesafen alone. The resistance index of the RCA accession, based on 50% biomass reduction, ranged from 63-fold (fomesafen alone) to 22-fold (malathion plus fomesafen), when compared with a 2007 susceptible, and 476-fold and 167-fold, respectively, relative to a 1986 susceptible check. The RCA accession was resistant to other protoporphyrinogen oxidase (PPO) inhibitors (i.e., flumioxazin, acifluorfen, saflufenacil) as well as the 4-hydroxyphenylpyruvate dioxygenase (HPPD) inhibitor tembotrione and acetolactate synthase (ALS) inhibitor pyrithiobac sodium. Sequencing of theALSgene revealed no point mutations, indicating that a target-site mechanism is not involved in conferring ALS-inhibitor resistance in the RCA accession. Of the three PPO-inhibiting herbicides tested in combination with the malathion, saflufenacil resulted in the greatest biomass reduction (80%;P< 0.05) and lowest survival rate (23%;P< 0.05) relative to nontreated plants. The application of cytochrome P450 or glutathioneS-transferase inhibitors with fomesafen did not lead to any adverse effects on soybean, suggesting a possible role for these compounds for management of NTSR under field conditions. These results shed light on the relative unpredictability of NTSR in conferring herbicide cross- and multiple resistance in Palmer amaranth.
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Lee, Chad D., Alex R. Martin, Fred W. Roeth, Blaine E. Johnson i Donald J. Lee. "Comparison of ALS inhibitor resistance and allelic interactions in shattercane accessions". Weed Science 47, nr 3 (czerwiec 1999): 275–81. http://dx.doi.org/10.1017/s0043174500091773.
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Reports of unacceptable shattercane (Sorghum bicolor) control with acetolactate synthase (ALS)-inhibiting herbicides prompted the investigation of 29 fields in central and south-central Nebraska for ALS-resistant (ALSr) shattercane. These fields were located in three distinct geographical areas designated C, G, and P. Shattercane from 13 fields spanning all three areas was resistant to 80 g ai ha−1(2 X field rate) primisulfuron. Accessions C and G were more resistant than accession P to primisulfuron and nicosulfuron. Accessions C and G were susceptible to imazethapyr, whereas accession P was resistant. The ALS resistance was associated with alterations in the ALS enzyme. Primisulfuron I50values for ALS from ROX (forage sorghum), C, G, and P were 7, 8,510, 8,870, and 714 nM, respectively; nicosulfuron I50values were 647, 4,110, 4,070, and 1,460 nM, respectively; and imazethapyr I50values were 5,440, 13,100, 11,800, and 51,700 nM, respectively. Based on cross-resistance and enzyme sensitivities, at least two biotypes are represented in the three accessions of ALSr shattercane. Shattercane individuals from accessions C, G, and P were intercrossed to determine if the ALSr genes in each of the accessions were at independent loci. All the F2populations were resistant to 80 g ai ha−1primisulfuron, suggesting that the ALSr alleles in the three accessions are at the same locus or possibly linked loci. When the C, G, and P accessions were crossed with the wild type (WT), comparisons between the F1, susceptible, and resistant populations showed that primisulfuron resistance was expressed as a dominant, partially dominant, and additive trait for the C, G, and P accessions, respectively. The differences in ALSr allelic interactions indicate that primisulfuron resistance developed independently in each of the three accessions.
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Beckie, Hugh J., Eric N. Johnson i Anne Légère. "Negative Cross-Resistance of Acetolactate Synthase Inhibitor–Resistant Kochia (Kochia scoparia) to Protoporphyrinogen Oxidase– and Hydroxyphenylpyruvate Dioxygenase–Inhibiting Herbicides". Weed Technology 26, nr 3 (wrzesień 2012): 570–74. http://dx.doi.org/10.1614/wt-d-12-00020.1.
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This greenhouse experiment examined the response of homozygous susceptible and acetolactate synthase (ALS) inhibitor–resistant plants from six Canadian kochia accessions with the Pro197 or Trp574 mutation to six alternative herbicides of different sites of action. The null hypothesis was ALS-inhibitor–resistant and –susceptible plants from within and across accessions would respond similarly to herbicides of different sites of action. This hypothesis was accepted for all accessions except that of MBK2 with the Trp574 mutation. Resistant plants of that accession were 80, 60, and 50% more sensitive than susceptible plants to pyrasulfotole, mesotrione (hydroxyphenylpyruvate dioxygenase [HPPD] inhibitors), and carfentrazone (protoporphyrinogen oxidase [PPO] inhibitor), respectively. However, no differential dose response between resistant and susceptible plants of this kochia accession to bromoxynil, fluroxypyr, or glyphosate was observed. A previous study had found marked differences in growth and development between resistant and susceptible plants of this accession, but not of the other accessions examined in this experiment. Negative cross-resistance exhibited by resistant plants of accession MBK2 to PPO and HPPD inhibitors in this experiment may be a pleiotropic effect related to the Trp574 mutation.
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Nakka, Sridevi, Curtis R. Thompson, Dallas E. Peterson i Mithila Jugulam. "Target Site–Based and Non–Target Site Based Resistance to ALS Inhibitors in Palmer Amaranth (Amaranthus palmeri)". Weed Science 65, nr 6 (20.09.2017): 681–89. http://dx.doi.org/10.1017/wsc.2017.43.
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Resistance to acetolactate synthase (ALS)-inhibitor herbicides due to continuous and repeated selection is widespread in many troublesome weed species, including Palmer amaranth, throughout the United States. The objective of this research was to investigate the physiological and molecular basis of resistance to ALS inhibitors in a chlorsulfuron-resistant Palmer amaranth population (KSR). Our results indicate that the KSR population exhibits a high level of resistance to chlorsulfuron compared with two known susceptible populations, MSS and KSS from Mississippi and Kansas, respectively. MSS is highly susceptible to chlorsulfuron, whereas KSS is moderately sensitive. Dose–response analysis revealed that KSR was more than 275-fold more resistant compared with KSS. Nucleotide sequence analysis of theALSgene from the plants that survived chlorsulfuron treatment revealed the possibility of evolution of both target site–based and non–target site based resistance to ALS inhibitors in the KSR population. The most common mutation (Pro-197-Ser) in theALSgene associated with resistance to the sulfonylureas in many weed species was found only in 30% of the KSR population. A preliminary malathion study showed that the remaining 70% of resistant plants might have cytochrome P450–mediated non–target site resistance. This is the first report elucidating the mechanism of resistance to ALS inhibitors in Palmer amaranth from Kansas. Presence of both target site– and non–target site based mechanisms of resistance limits the herbicide options to manage Palmer amaranth in cropping systems.
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Zhao, Ning, Yaling Bi, Cuixia Wu, Dandan Wang, Ludan You, Weitang Liu i Jinxin Wang. "Cross-resistance to acetolactate synthase (ALS) inhibitors associated with different mutations in Japanese foxtail (Alopecurus japonicus)". Weed Science 67, nr 4 (31.05.2019): 389–96. http://dx.doi.org/10.1017/wsc.2019.15.
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AbstractJapanese foxtail (Alopecurus japonicus Steud.) is an invasive grass weed that severely threatens the production of wheat (Triticum aestivum L.) and canola (Brassica napus L.) crops in eastern Asia. Mesosulfuron-methyl is a highly efficient acetolactate synthase (ALS)-inhibiting herbicide widely used for control of this species in China. However, in recent years, some A. japonicus populations have evolved resistance to mesosulfuron-methyl by different amino acid substitutions (AASs) within the ALS gene. In the current study, 11 populations of A. japonicus were collected from Anhui Province, China, where the wheat fields were severely infested with this weed. Based on single-dose screening, eight of these populations evolved resistance to mesosulfuron-methyl, and gene sequencing revealed three AASs located in codon 197 or 574 of the ALS gene in the different resistant populations. Subsequently, three typical populations, AH-1, AH-4, and AH-10 with Trp-574-Leu, Pro-197-Thr, and Pro-197-Ser mutations, respectively, in ALS genes were selected to characterize their cross-resistance patterns to ALS inhibitors. Compared with the susceptible population AH-S, AH-1 showed broad-spectrum cross-resistance to sulfonylureas (SUs), imidazolinones (IMIs), triazolopyrimidines (TPs), and sulfonyl-aminocarbonyl-triazolinones (SCTs); whereas AH-4 and AH-10 were resistant to SUs, TPs, and SCTs but sensitive to IMIs. Moreover, all three resistant populations were sensitive to both photosystem II inhibitor isoproturon and 4-hydroxyphenylpyruvate dioxygenase inhibitor QYM201 (1-(2-chloro-3-(3-cyclopropyl-5-hydroxy-1-methyl-1H-pyrazole-4-carbonyl)-6-(trifluoromethyl)phenyl)piperidin-2-one). Based on the current state of knowledge, this study is the first report of A. japonicus evolving cross-resistance to ALS-inhibiting herbicides due to a Pro-197-Ser mutation in the ALS gene.
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McCullough, Patrick E., Jialin Yu, J. Scott McElroy, S. Chen, H. Zhang, Timothy L. Grey i Mark A. Czarnota. "ALS–Resistant Annual Sedge (Cyperus compressus) Confirmed in Turfgrass". Weed Science 64, nr 1 (marzec 2016): 33–41. http://dx.doi.org/10.1614/ws-d-15-00094.1.
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Acetolactate synthase (ALS) inhibitors are widely used for POST control of sedges in turfgrass. A suspected resistant (R) biotype of annual sedge was collected from a bermudagrass turf in Georgia with a history of exclusive use of halosulfuron. Research was conducted to evaluate the resistance level of this biotype to halosulfuron, efficacy of ALS-inhibiting herbicides and other mechanisms of action for control, and the molecular and physiological basis for resistance. In greenhouse experiments, the halosulfuron rate required to reduce shoot biomass 50% in comparison with the nontreated at 8 wk after treatment (WAT) were 8 and > 1,120 g ai ha−1for the S (susceptible) and R biotypes, respectively. Imazapic, sulfosulfuron, and trifloxysulfuron reduced biomass of the S biotype greater than 60% at 8 WAT, but biomass was reduced less than 20% for the R biotype. Glufosinate, glyphosate, MSMA, and sulfentrazone reduced shoot biomass of the R biotype by 93, 86, 97, and 45%, respectively. In laboratory experiments, the halosulfuron concentration required to inhibit ALS activity by 50% in excised leaf tissues was 5.8 and > 1,000 μM for the S and R biotypes, respectively. Gene sequencing of the R biotype revealed a Pro-197-Ser substitution that confers resistance to ALS inhibitors. This is the first report of ALS-inhibitor resistance in annual sedge and herbicide resistance in a sedge species from a turfgrass system.
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Hoyos, Verónica, Guido Plaza, José G. Vázquez-Garcia, Candelario Palma-Bautista, Antonia M. Rojano-Delgado i Rafael De Prado. "Confirmation of Multiple Resistant Chloris radiata Population, Harvested in Colombian Rice Fields". Agronomy 11, nr 3 (6.03.2021): 496. http://dx.doi.org/10.3390/agronomy11030496.
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This paper reports the first C. radiata population with resistance to glyphosate and multiple resistance to the acetolactate synthase (ALS) inhibitor, imazamox. Two populations, one putative resistant (R) and one susceptible (S), were used in the studies. Dose–response experiments were performed to evaluate the resistance factor (RF). Shikimic acid accumulation, 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) and ALS enzyme activities were studied together with chemical integrated weed management (adjuvants and alternative herbicides). The resistance to glyphosate and imazamox was confirmed based on the dry weight reduction, visual evaluation and survival. The results of dose–response curve assays showed for the R population intermedium RF for glyphosate (5.1 and 9.7 for amount of herbicide needed to reduce the dry weight by 50% GR50 and lethal dose of 50% LD50, respectively) and high RF for imazamox (34.9 and 37.4, respectively). The low shikimic acid accumulation in R population confirmed the glyphosate resistance. The glyphosate concentration which inhibited the EPSPS enzyme in 50% (I50) was approximately 20 times higher for R population than the S population, while the imazamox I50 in ALS enzyme for the R plants was 89 times greater than the S plants. In the chemical integrated weed management, the foliar retention and effectivity assays showed that the use of adjuvants improves the retention of glyphosate and imazamox, and the reduction in dry weight of weeds. The alternative herbicides study showed that the acetyl-CoA carboxylase (ACCase) inhibitors, paraquat and glufosinate, had better results for control in this species. However, poor control was observed with bispyribac-sodium, metsulfuron-methyl and quinclorac, indicating possible cross-resistance for ALS-inhibitors and also multiple resistance for auxinic herbicides (quinclorac). Nevertheless dose–response experiments are required to confirm this assumption.
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Evans, Cody M., Seth A. Strom, Dean E. Riechers, Adam S. Davis, Patrick J. Tranel i Aaron G. Hager. "Characterization of a waterhemp (Amaranthus tuberculatus) population from Illinois resistant to herbicides from five site-of-action groups". Weed Technology 33, nr 03 (23.05.2019): 400–410. http://dx.doi.org/10.1017/wet.2019.19.
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AbstractExperiments were initiated to characterize a waterhemp population (CHR) discovered in a central Illinois corn field after it was not controlled by the 4-hydroxyphenylpyruvate dioxygenase (HPPD) inhibitor topramezone. Field experiments conducted during 2014–2015 indicated that acetolactate synthase (ALS)-, protoporphyrinogen oxidase (PPO)-, photosystem II (PSII)-, and HPPD-inhibiting herbicides and the synthetic auxin 2,4-D did not control the CHR population. Laboratory experiments confirmed target site–based resistance mechanisms to ALS- and PPO-inhibiting herbicides. Herbicide doses required to reduce dry biomass 50% (GR50) were determined in greenhouse dose–response experiments, and indicated 16-fold resistance to the HPPD inhibitor mesotrione, 9.5-fold resistance to the synthetic auxin 2,4-D, and 252-fold resistance to the PSII inhibitor atrazine. Complementary results from field, laboratory, and greenhouse investigations indicate that the CHR population has evolved resistance to herbicides from five sites of action (SOAs): ALS-, PPO-, PSII-, and HPPD-inhibiting herbicides and 2,4-D. Herbicide use history for the field in which CHR was discovered indicates no previous use of 2,4-D.
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Gaeddert, Jason W., Dallas E. Peterson i Michael J. Horak. "Control and Cross-Resistance of an Acetolactate Synthase Inhibitor-Resistant Palmer Amaranth (Amaranthus palmeri) Biotype". Weed Technology 11, nr 1 (marzec 1997): 132–37. http://dx.doi.org/10.1017/s0890037x00041464.
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Over two years, acetolactate synthase (ALS)-inhibiting herbicides and herbicides with different mechanisms of action were tested individually and in combination for control of ALS-resistant Palmer amaranth in soybean. As expected, ALS-inhibiting herbicides did not control the resistant Palmer amaranth. Lactofen at 210 g/ha and acifluorfen at 560 g/ha gave the best postemergence control. Tank mixes of lactofen with either imazethapyr or chlorimuron plus thifensulfuron did not significantly increase control over lactofen alone. Sequential treatment with a soil-applied herbicide, either SAN 582 or pendimethalin, followed by lactofen postemergence, controlled weeds best (greater than 85%). The extent of cross-resistance of Palmer amaranth to ALS-inhibiting herbicides was determined in the greenhouse. Sixteen POST ALS-inhibiting herbicides were sprayed at ½, 1, 2, 4, and 8X field use rates on resistant and susceptible biotypes. All ALS-inhibiting herbicides at all rates controlled the susceptible biotype. The resistant biotype was cross-resistant to all ALS-inhibiting herbicides. Metsulfuron and imazapyr at 8X rates were the only treatments that provided 80% or greater control of the ALS-resistant Palmer amaranth. Chlorsulfuron and tribenuron were the only other herbicides that gave partial control at the highest rate. Control with these four herbicides decreased as the rate was decreased. Experimental results suggest that cultural practices and herbicides with different mechanisms of action will be required to manage this ALS-resistant Palmer amaranth biotype.
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Warwick, Suzanne I., Connie A. Sauder i Hugh J. Beckie. "Acetolactate Synthase (ALS) Target-Site Mutations in ALS Inhibitor-Resistant Russian Thistle (Salsola tragus)". Weed Science 58, nr 3 (wrzesień 2010): 244–51. http://dx.doi.org/10.1614/ws-d-09-00083.1.
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ALS inhibitor-resistant biotypes are the fastest growing class of herbicide-resistant (HR) weeds. A Canadian ALS inhibitor-resistant biotype of Russian thistle was first reported in 1989. The molecular basis for ALS-inhibitor resistance is unknown for Canadian populations of this polyploid weed species, and was determined in this study for one Alberta and two Saskatchewan HR Russian thistle populations. HR plants survived spray application of the ALS-inhibitor mixture thifensulfuron : tribenuron in the greenhouse. All three HR Russian thistle populations were heterogeneous and contained both HR and herbicide-susceptible (HS) individuals. The molecular basis for resistance was determined by sequencing theALSgene and/or conducting a TaqMan genotyping assay for single nucleotide polymorphism (SNP) for the Trp574Leu mutation. Two target-site mutations were observed: Trp574Leu in all three biotypes (554 individuals) and Pro197Gln in one biotype (one individual), suggesting multiple-founding events for Russian thistle HR populations in western Canada. Segregation patterns among F1 and F2 progeny arrays of HR lines sprayed under greenhouse conditions varied; some segregated (i.e., had HR and HS progeny), whereas other lines were exclusively HR. In contrast, no segregation of molecular types, i.e., Trp574, Trp/Leu574and Leu574, as would be expected with heterozygosity at a single locus Trp/Leu574, was observed. Such lack of segregation is consistent with the polyploid genome structure of Russian thistle and the presence of two copies of theALSgene. The presence of more than oneALSgene confounded the ability of the molecular techniques to accurately identify “true” heterozygotes in this study.
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Ferguson, Gabrielle M., Allan S. Hamill i François J. Tardif. "ALS inhibitor resistance in populations of Powell amaranth and redroot pigweed". Weed Science 49, nr 4 (lipiec 2001): 448–53. http://dx.doi.org/10.1614/0043-1745(2001)049[0448:airipo]2.0.co;2.
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White, Anthony D., Michelle A. Graham i Micheal D. K. Owen. "Isolation of acetolactate synthase homologs in common sunflower". Weed Science 51, nr 6 (grudzień 2003): 845–53. http://dx.doi.org/10.1614/p2002-136.
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A common sunflower population from Howard, SD (HSD) was previously determined to be cross-resistant to imazethapyr and chlorimuron-ethyl, both acetolactate synthase–inhibiting (ALS) herbicides. Experiments were conducted to determine if target-site polymorphisms could act as a mechanism of ALS-inhibitor herbicide resistance in the HSD common sunflower. Approximately 1,600 nucleotides were amplified by polymerase chain reaction and sequenced from putativeALSgene(s) in common sunflower and Jerusalem artichoke. In sunflower, two different amplification products were detected that differed by a nine-basepair deletion. This suggested the presence of at least two ALS genes in common sunflower that could contribute to the herbicide resistance phenotype. In addition, an Ala205to Val205substitution was observed in several clones from resistant common sunflower (amino acid position is relative to the full-length mouse-ear cress ALS protein). Previously documented mutations at this position in other species indicated that it might play a vital role in conferring resistance to one or more ALS-inhibitor herbicides.
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Manley, Brian S., Bijay K. Singh, Dale L. Shaner i Henry P. Wilson. "Imidazolinone Resistance in Smooth Pigweed (Amaranthus hybridus) Is Due to an Altered Acetolactate Synthase". Weed Technology 13, nr 4 (grudzień 1999): 697–705. http://dx.doi.org/10.1017/s0890037x0004210x.
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Seeds were collected from an imidazolinone-resistant (R) population of smooth pigweed near Marion, MD, and from an imidazolinone-susceptible (S) population near Painter, VA, and grown in the greenhouse. Acetolactate synthase (ALS) enzyme was extracted from both biotypes and assayed in the presence of CGA 152005, chlorimuron, halosulfuron, imazaquin, imazethapyr, nicosulfuron, primisulfuron, pyrithiobac, rimsulfuron, and thifensulfuron to determine if an altered ALS was the mechanism of resistance in the R biotype and to determine if this biotype was cross-resistant to other ALS inhibitor herbicides. The inhibitor concentration required to cause a 50% reduction in ALS activity (I50) was calculated for each herbicide. ALS from the R biotype was approximately 71-, 109,000-, and 9-fold more resistant to imazaquin, imazethapyr, and rimsulfuron, respectively, than that from the S biotype. ALS from the R biotype was approximately threefold more sensitive to pyrithiobac and thifensulfuron than that from the S biotype. R ALS was also slightly more tolerant to CGA 152005 and nicosulfuron and slightly more sensitive to primisulfuron and chlorimuron. ALS from both biotypes generally responded similarly to halosulfuron. Resistance in the R biotype was due to an altered form of ALS that is insensitive to the imidazolinone herbicides and rimsulfuron.
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Gerwick, B. Clifford, Linda C. Mireles i Robert J. Eilers. "Rapid Diagnosis of Als/Ahas-Resistant Weeds". Weed Technology 7, nr 2 (czerwiec 1993): 519–24. http://dx.doi.org/10.1017/s0890037x00027986.
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A method to rapidly identify acetolactate synthase/acetohydroxyacid synthase (ALS/AHAS)-resistant weeds is described based upon the differential accumulation of acetoin in the presence and absence of an ALS/AHAS inhibitor herbicide. Acetoin accumulation is induced by inhibition of ketol-acid reductoisomerase (KARI), the enzyme immediately following ALS/AHAS in the biosynthesis of branched-chain amino acids. Inhibition of ALS/AHAS prevents the build up of acetoin and forms the basis for distinguishing between sensitive and resistant biotypes. A new inhibitor of KARI, 1,1-cyclopropanedicarboxylic acid (CPCA), is described and was found to cause acetoin accumulation in velvetleaf leaf disks over the concentration range of 2 to 100 000 μM. In the presence of CPCA, a number of species important to monitor for ALS/AHAS resistance were found to accumulate acetoin at rates sufficient for resistance diagnosis in 2 to 8 h. In velvetleaf, the youngest apical leaf was found to be the most active in acetoin accumulation. The resistance diagnosis method was validated by clearly distinguishing between imazaquin-sensitive and imazaquin-resistant cocklebur biotypes.
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Beckie, Hugh J., Suzanne I. Warwick, Connie A. Sauder, Chris Lozinski i Scott Shirriff. "Occurrence and Molecular Characterization of Acetolactate Synthase (ALS) Inhibitor–Resistant Kochia (Kochia scoparia) in Western Canada". Weed Technology 25, nr 1 (marzec 2011): 170–75. http://dx.doi.org/10.1614/wt-d-10-00067.1.
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A survey of 109 fields was conducted across western Canada in spring 2007 to determine the extent of ALS-inhibitor and dicamba (synthetic auxin) resistance in kochia. Weed seedlings were collected from fields in three provinces of western Canada and transplanted into the greenhouse. Seeds were harvested from selfed plants, and the F1progeny were screened for resistance to the ALS-inhibitor mixture thifensulfuron–tribenuron or dicamba. All kochia populations were susceptible to dicamba. ALS inhibitor–resistant kochia was found in 85% of the fields surveyed in western Canada: 80 of 95 fields in Alberta, six of seven fields in Saskatchewan, and all seven fields in Manitoba. For the 93 ALS inhibitor–resistant populations, the mean frequency (±SE) of parental plants classified as resistant was 61 ± 3%. Most of the resistant populations (87%) were heterogeneous and contained both resistant and susceptible individuals.ALSsequence data (Pro197and Asp376mutations) and genotyping data (Trp574mutation) obtained for 87 kochia parental (i.e., field-collected) plants confirmed the presence of all three target-site mutations as well as two mutational combinations (Pro197+ Trp574, Asp376+ Trp574) in resistant individuals.
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Warwick, Suzanne I., Connie Sauder i Hugh J. Beckie. "Resistance in Canadian biotypes of wild mustard (Sinapis arvensis) to acetolactate synthase inhibiting herbicides". Weed Science 53, nr 5 (październik 2005): 631–39. http://dx.doi.org/10.1614/ws-05-003r1.1.
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Multiple cases of ALS inhibitor-resistant weed biotypes are reported for many species, including wild mustard. The physiological extent and molecular basis of resistance to ALS inhibitors was compared in four biotypes of wild mustard from western Canada: a sulfonylurea (SU)-resistant (R) biotype from Manitoba detected in 1992; an SU (ethametsulfuron)-R biotype from Alberta detected in 1993 (metabolism-based resistance); an SU-R biotype from Manitoba detected in 2002; and a SU- and imidazolinone (IMI)-R biotype from Saskatchewan detected in 2002. Herbicide dose-response experiments confirmed that the two Manitoba biotypes were resistant to the SU herbicides ethametsulfuron and tribenuron : thifensulfuron mixture, whereas the Saskatchewan biotype was resistant to both SU herbicides and to imazethapyr, an IMI herbicide. Sequence analysis of theALSgene detected target site mutations in three of the four R biotypes, with amino acid substitutions Pro197(CCT) to Ser (TCT) [Domain A of the gene] in the two SU-R Manitoba biotypes and Trp574(TGG) to Leu (TTG) [Domain B] in the Saskatchewan biotype. The Alberta SU-R biotype had the sameALSnucleotide and amino acid sequence as the susceptible population at these two positions. Two heterozygous individuals [Trp574(Tt/gG)] were detected in the Saskatchewan biotype, and genetic segregation for nucleotide bases and resistance phenotype was consistent with single gene control. Nucleotide variation in neutral regions of theALSgene varied with biotype, with no variation in the two Manitoba biotypes, two variants in the Saskatchewan biotype, and 16 neutral nucleotide polymorphisms (0.9%) in the Alberta biotype. The occurrence of at least three different ALS inhibitor-R biotypes in this important weed species is likely to impact negatively on the use of ALS inhibitors, such as the IMIs, and serves as a warning for strict implementation of herbicide rotations to prevent or delay the evolution and spread of such populations.
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Bell, Michael S., Aaron G. Hager i Patrick J. Tranel. "Multiple Resistance to Herbicides from Four Site-of-Action Groups in Waterhemp (Amaranthus tuberculatus)". Weed Science 61, nr 3 (wrzesień 2013): 460–68. http://dx.doi.org/10.1614/ws-d-12-00166.1.
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In 2006 and 2007, farmers from two counties in Illinois reported failure to control waterhemp with glyphosate. Subsequent onsite field experiments revealed that the populations might be resistant to multiple herbicides. Greenhouse experiments therefore were conducted to confirm glyphosate resistance, and to test for multiple resistance to other herbicides, including atrazine, acifluorfen, lactofen, and imazamox. In glyphosate dose-response experiments, both populations responded similarly to a previously characterized glyphosate-resistant population (MO1). Both Illinois populations also demonstrated high frequencies of resistance to the acetolactate synthase (ALS) inhibitor, imazamox. Additionally, one of the populations demonstrated high frequencies of resistance to both atrazine and the protoporphyrinogen oxidase (PPO) inhibitor, lactofen. Furthermore, using combinations of sequential and tank-mix herbicide applications, individual plants resistant to herbicides spanning all four site-of-action groups were identified from one population. Molecular experiments were performed to provide an initial characterization of the resistance mechanisms and to provide confirmation of the presence of multiple resistance traits within the two populations. Both populations contained the W574L ALS mutation and the ΔG210 PPO mutation, previously shown to confer resistance to ALS and PPO inhibitors, respectively. Atrazine resistance in both populations is suspected to be metabolism-based, because a triazine target-site mutation was not identified. A P106S EPSPS mutation, previously reported to confer glyphosate resistance, was identified in one population. This mutation was identified in both resistant and sensitive plants from the population; however, and so more research is needed to determine the glyphosate-resistance mechanism(s). This is the first known case of a weed population in the United States possessing multiple resistance to herbicides from four site-of-action groups.
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Schultz, John L., Laura A. Chatham, Chance W. Riggins, Patrick J. Tranel i Kevin W. Bradley. "Distribution of Herbicide Resistances and Molecular Mechanisms Conferring Resistance in Missouri Waterhemp (Amaranthus rudisSauer) Populations". Weed Science 63, nr 1 (marzec 2015): 336–45. http://dx.doi.org/10.1614/ws-d-14-00102.1.
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A survey of soybean fields containing waterhemp was conducted just prior to harvest in 2012 to determine the scope and extent of herbicide resistance and multiple herbicide resistances among a sample of Missouri waterhemp populations. Resistance was confirmed to glyphosate and to acetolactate synthase (ALS), protoporphyrinogen oxidase (PPO), photosystem II (PSII), and 4-hydroxyphenylpyruvate dioxygenase (HPPD) inhibitors, but not to 2,4-D. Of the 187 populations tested, 186 exhibited resistance to chlorimuron. The proportions of populations with atrazine or glyphosate resistance were similar, with 30 and 29% of the populations surviving the 3× rates. Lactofen resistance was observed in 5% of the populations, whereas mesotrione resistance was only found in 1.6% of the populations. All populations tested were susceptible to 2,4-D at the 3× rate. At least 52% of the waterhemp populations tested exhibited resistance to herbicides from two mechanism of action. Resistance to atrazine plus chlorimuron as well as glyphosate plus chlorimuron was present in 29% of the populations. Three-way resistance, primarily comprised of resistance to atrazine plus chlorimuron plus glyphosate, was present in 11% of the populations. Resistance to herbicides from four mechanisms of action was found in 2% of the populations, and one population exhibited resistance to herbicides from five mechanisms of action. DNA analysis of a subsample of plants revealed that previously documented mechanisms of resistance in waterhemp, including the ΔG210 deletion conferring PPO-inhibitor resistance, the Trp574Leu amino acid substitution conferring ALS-inhibitor resistance, and elevated 5-enolypyruvyl-shikimate-3-phosphate synthase copy number and the Pro106Ser amino acid substitution resulting in glyphosate resistance, explained survival in many, but not all, instances. Atrazine resistance was not explained by the Ser264Gly D1 protein substitution. Overall, results from these experiments indicate that Missouri soybean fields contain waterhemp populations with resistance to glyphosate, ALS-, PPO-, PSII-, and HPPD-inhibiting herbicides, which are some of the most common mechanisms of action currently utilized for the control of this species in corn and soybean production systems. Additionally, these results indicate that slightly more than half of the populations tested exhibit resistance to more than one herbicide mechanisms of action. Managing the current resistance levels in existing populations is of utmost importance. The use of multiple, effective herbicide modes of action, both preemergence and postemergence, and the integration of optimum cultural and mechanical control practices will be vital in the management of Missouri waterhemp populations in the future.
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EBERHARDT, D. S., A. M. OLIVEIRA NETO, J. A. NOLDIN i R. M. VANTI. "Barnyardgrass with Multiple Resistance to Synthetic Auxin, ALS and Accase Inhibitors". Planta Daninha 34, nr 4 (grudzień 2016): 823–32. http://dx.doi.org/10.1590/s0100-83582016340400023.
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ABSTRACT The objective of this research was to confirm the resistance of a barnyardgrass biotype (Echinochloa crus-galli) to herbicides quinclorac (synthetic auxin), penoxsulam (ALS inhibitor) and cyhalofop-butyl (ACCase inhibitor). Two experiments were carried out in a greenhouse located in Itajaí, State of Santa Catarina, Brazil. One experiment evaluating the biotype ECH 18 (known as susceptible) and one with the ECH 141 biotype (suspected to be multiple resistant). The experimental design used was completely randomized, in a 4 x 7 factorial arrangement with four replications. The first factor was the herbicide: cyhalofop-butyl (Clincher(r)), penoxsulam (Ricer(r)), quinclorac (Facet(r)) and propanil (Grassaid(r)) and the second factor consisting of seven rates of each herbicide (0.00; 0.25; 0.50; 1; 2; 4 and 8 times the label rate). The evaluations of percentage of control, plant density per pot and dry mass of shoots were performed 35 days after treatments. The rates to control 50% and 80% and the dose to provide 50% and 80% of the weed biomass accumulation and the resistance factor were estimated based on data analysis. The initial hypothesis was confirmed; the biotype ECH 141 presented multiple resistance (synthetic auxin, ALS and ACCase inhibitor). However, the herbicide propanil controlled biotype ECH 141 adequate.
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Beckie, Hugh J., Suzanne I. Warwick, Connie A. Sauder, Gina M. Kelln i Chris Lozinski. "Acetolactate Synthase Inhibitor–Resistant False Cleavers (Galium spurium) in Western Canada". Weed Technology 26, nr 1 (marzec 2012): 151–55. http://dx.doi.org/10.1614/wt-d-11-00075.1.
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Cleavers species (false cleavers and catchweed bedstraw) are among the top 10 most abundant weeds across the prairie region of western Canada, and are increasing in relative abundance at the fastest rate since the 1970s. In 2008, two false cleavers populations from Tisdale and Choiceland, Saskatchewan, were suspected of acetolactate synthase (ALS) –inhibitor resistance. Dose-response experiments were conducted with the use of imazethapyr and florasulam, both ALS inhibitors, as well as fluroxypyr, a synthetic auxin. Additionally, a 1,954–base-pair region of theALSgene including sites known to conferALSresistance were sequenced. Both populations were highly resistant to imazethapyr (resistance factors greater than 100), one population (Tisdale) was highly resistant to florasulam (Choiceland population susceptible, although a second, larger screening of 200 individuals indicated low frequency [2%] florasulam resistance), and both populations were susceptible to fluroxypyr. All sequenced Tisdale individuals screened with imazethapyr posessed the Trp574Leu mutation. In contrast, three point mutations were found for Choiceland individuals sequenced: Ser653Asn, Trp574Leu, and Asp376Glu. TheseALStarget-site mutations have not been documented previously in this species.
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Beckie, Hugh J., Robert E. Blackshaw, Ryan Low, Linda M. Hall, Connie A. Sauder, Sara Martin, Randall N. Brandt i Scott W. Shirriff. "Glyphosate- and Acetolactate Synthase Inhibitor–Resistant Kochia (Kochia scoparia) in Western Canada". Weed Science 61, nr 2 (czerwiec 2013): 310–18. http://dx.doi.org/10.1614/ws-d-12-00140.1.
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In summer, 2011, we investigated suspected glyphosate-resistant (GR) kochia in three chem-fallow fields (designated F1, F2, F3, each farmed by a different grower) in southern Alberta. This study characterizes glyphosate resistance in those populations, based on data from dose–response experiments. In a greenhouse experiment, the three populations exhibited a resistance factor ranging from 4 to 6 based on shoot biomass response (GR50ratios), or 5 to 7 based on survival response (LD50ratios). Similar results were found in a field dose–response experiment at Lethbridge, AB, in spring 2012 using the F2 kochia population. In fall 2011, we surveyed 46 fields within a 20-km radius of the three chem-fallow fields for GR kochia. In the greenhouse, populations were screened with glyphosate at 900 g ae ha−1. Seven populations were confirmed as GR, the farthest site located about 13 km from the three originally confirmed populations. An additional GR population more than 100 km away was later confirmed. Populations were screened for acetolactate synthase (ALS)–inhibitor (thifensulfuron : tribenuron) and dicamba resistance in the greenhouse, with molecular characterization of ALS-inhibitor resistance in the F1, F2, and F3 populations. All GR populations were resistant to the ALS-inhibiting herbicide, but susceptible to dicamba. ALS-inhibitor resistance in kochia was conferred by Pro197, Asp376, or Trp574amino acid substitutions. Based upon a simple empirical model with a parameter for selection pressure, calculated from weed relative abundance and glyphosate efficacy, and a parameter for seedbank longevity, kochia, wild oat, and green foxtail were the top three weeds, respectively, predicted at risk of selection for glyphosate resistance in the semiarid Grassland region of the Canadian prairies; wild oat, green foxtail, and cleavers species were predicted at greatest risk in the subhumid Parkland region. This study confirms the first occurrence of a GR weed in western Canada. Future research on GR kochia will include monitoring, biology and ecology, fitness, mechanism of resistance, and best management practices.
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Tehranchian, Parsa, Vijay K. Nandula, Maor Matzrafi i Marie Jasieniuk. "Multiple herbicide resistance in California Italian ryegrass (Lolium perenne ssp. multiflorum): characterization of ALS-inhibiting herbicide resistance". Weed Science 67, nr 3 (29.03.2019): 273–80. http://dx.doi.org/10.1017/wsc.2019.1.
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AbstractMultiple resistance to glyphosate, sethoxydim, and paraquat was previously confirmed in two Italian ryegrass [Lolium perenne L. ssp. multiflorum (Lam.) Husnot] populations, MR1 and MR2, in northern California. Preliminary greenhouse studies revealed that both populations were also resistant to imazamox and mesosulfuron, both of which are acetolactate synthase (ALS)-inhibiting herbicides. In this study, three subpopulations, MR1-A (from seed of MR1 plants that survived a 16X rate of sethoxydim), MR1-P (from seed of MR1 plants that survived a 2X rate of paraquat), and MR2 (from seed of MR2 plants that survived a 16X rate of sethoxydim), were investigated to determine the resistance level to imazamox and mesosulfuron, evaluate other herbicide options for the control of these multiple resistant L. perenne ssp. multiflorum, and characterize the underlying ALS-inhibitor resistance mechanism(s). Based on LD50 values, the MR1-A, MR1-P, and MR2 subpopulations were 38-, 29-, 8-fold and 36-, 64-, and 3-fold less sensitive to imazamox and mesosulfuron, respectively, relative to the susceptible (Sus) population. Only MR1-P and MR2 plants were cross-resistant to rimsulfuron, whereas both MR1 subpopulations were cross-resistant to imazethapyr. Pinoxaden (ACCase inhibitor [phenylpyrazoline 'DEN']) only controlled MR2 and Sus plants at the labeled field rate. However, all plants were effectively controlled (>99%) with the labeled field rate of glufosinate. Based on I50 values, MR1-A, MR-P, and MR2 plants were 712-, 1,104-, and 3-fold and 10-, 18-, and 5-fold less responsive to mesosulfuron and imazamox, respectively, than the Sus plants. Sequence alignment of the ALS gene of resistant plants revealed a missense single-nucleotide polymorphism resulting in a Trp-574-Leu substitution in MR1-A and MR1-P plants, heterozygous in both, but not in the MR2 plants. An additional homozygous substitution, Asp-376-Glu, was identified in the MR1-A plants. Addition of malathion or piperonyl butoxide did not alter the efficacy of mesosulfuron on MR2 plants. In addition, the presence of 2,4-D had no effect on the response of mesosulfuron on the MR2 and Sus. These results suggest an altered target site is the mechanism of resistance to ALS inhibitors in MR1-A and MR1-P plants, whereas a non–target site based resistance apparatus is present in the MR2 plants.