Differential Herbicide Response Among Sulfonylurea-Resistant Kochia scoparia L. Accessions

Weed Science ◽  
1993 ◽  
Vol 41 (2) ◽  
pp. 159-165 ◽  
Author(s):  
K. Sivakumaran ◽  
D. Mulugeta ◽  
P. K. Fay ◽  
W. E. Dyer

Three chlorsulfuron-resistant kochia accessions were tested for levels of resistance to sulfonylurea and imidazolinone herbicides, based on whole plant response and sensitivity of the target enzyme. The resistant Minot and Chester accessions were not affected by treatment with 175 g ha−1 chlorsulfuron, and I50 values for the Chester accession ranged from 22-fold (metsulfuron-methyl) to 196-fold (chlorsulfuron) higher than the susceptible Bozeman accession. However, the Chester accession was 1.5- to 2-fold more resistant than Minot to five sulfonylurea herbicides, as determined by acetolactate synthase (ALS) I50 values. The third resistant accession (Power) displayed an intermediate response and was only 2- to 5-fold more resistant than the susceptible Bozeman accession to all sulfonylurea herbicides tested. The Minot and Chester accessions were slightly cross-resistant to four imidazolinone herbicides, ranging from 2-fold (imazamethabenz, imazethapyr, and imazaquin) to 6-fold (imazapyr) more resistant than the Bozeman accession, but cross-resistance levels did not differ appreciably between the Minot and Chester accessions. The Power accession was not cross-resistant to the four imidazolinone herbicides tested. The results demonstrate that degrees of ALS resistance and cross-resistance are highly variable among kochia populations: these differences may be due to the type of mutation in the gene encoding ALS.

Weed Science ◽  
1999 ◽  
Vol 47 (1) ◽  
pp. 20-27 ◽  
Author(s):  
Matthew J. Foes ◽  
Lixin Liu ◽  
Gerald Vigue ◽  
Edward W. Stoller ◽  
Loyd M. Wax ◽  
...  

A kochia biotype from McDonough County, Illinois, was suspected to be resistant to both triazine and acetolactate synthase (ALS)-inhibiting herbicides. We performed greenhouse and laboratory experiments to confirm, quantify, and determine the molecular basis of multiple herbicide resistance in this biotype. Whole-plant phytotoxicity assays confirmed that the biotype was resistant to triazine (atrazine), imidazolinone (imazethapyr), and sulfonylurea (thifensulfuron and chlorsulfuron) herbicides. Relative to a susceptible kochia biotype, resistance to these herbicides ranged from 500- to > 28,000-fold. The kochia biotype from McDonough County also displayed high levels of resistance (2,000- to 9,000-fold) to ALS-inhibiting herbicides in in vivo ALS enzyme assays, indicating that resistance to these herbicides was site-of-action mediated. Results from chlorophyll fluorescence assays indicated that triazine resistance was also site-of-action mediated. Foliar applications of atrazine had little or no effect on photosynthesis in the resistant biotype, even when atrazine concentrations were 108-fold higher than needed to inhibit photosynthesis in the susceptible biotype. A region of the gene encoding the D1 protein of photosystem II and all of the open reading frame of the gene encoding ALS were sequenced and compared between the resistant and susceptible biotypes. Resistance to triazine and ALS-inhibiting herbicides in the kochia biotype from McDonough County was conferred by, respectively, a glycine for serine substitution at residue 264 of the D1 protein and a leucine for tryptophan substitution at residue 570 of ALS.


Weed Science ◽  
1998 ◽  
Vol 46 (1) ◽  
pp. 8-12 ◽  
Author(s):  
Terry R. Wright ◽  
Donald Penner

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


Weed Science ◽  
1997 ◽  
Vol 45 (2) ◽  
pp. 192-197 ◽  
Author(s):  
Christy L. Sprague ◽  
Edward W. Stoller ◽  
Loyd M. Wax ◽  
Michael J. Horak

Imazethapyr-resistant biotypes of Palmer amaranth and common waterhemp were studied to determine the magnitude of resistance and cross-resistance to three acetolactate synthase (ALS)-inhibiting herbicides. Resistant biotypes of Palmer amaranth and common waterhemp demonstrated > 2,800- and > 130-fold resistance to phytotoxicity of imazethapyr compared to susceptible biotypes, respectively. Concentrations of imazethapyr required for 50% in vivo inhibition of ALS activity were at least > 13,100 and > 1,900 times greater for resistant biotypes of Palmer amaranth and common waterhemp, respectively, compared to susceptible plants. Resistant biotypes of both species demonstrated cross-resistance to the sulfonylurea herbicides thifensulfuron and chlorimuron at the whole plant and enzyme levels, indicating that a less sensitive ALS enzyme confers this resistance to these plants.


1997 ◽  
Vol 11 (2) ◽  
pp. 241-247 ◽  
Author(s):  
Christy L. Sprague ◽  
Edward W. Stoller ◽  
Loyd M. Wax

Five biotypes of common cocklebur that were not controlled with acetolactate synthase (ALS)-inhibiting herbicides were tested in greenhouse and laboratory studies to determine the magnitude of resistance and cross-resistance to four ALS-inhibiting herbicides. In vivo inhibition of ALS was also evaluated. Based on phytotoxicity, all five ALS-resistant biotypes of common cocklebur were > 390 times more resistant than the susceptible biotype to imazethapyr. However, only four of these biotypes were also resistant to another imidazolinone, imazaquin. Two biotypes were cross-resistant to the sulfonylurea, chlorimuron, and the triazolopyrimidine sulfonanilide, NAF-75. One biotype demonstrated intermediate susceptibility to imazaquin, chlorimuron, and NAF-75. In all cases, the resistance exhibited at the whole plant level was associated with an insensitive ALS.


Weed Science ◽  
1996 ◽  
Vol 44 (4) ◽  
pp. 789-794 ◽  
Author(s):  
Sarah Taylor Lovell ◽  
Loyd M. Wax ◽  
Michael J. Horak ◽  
Dallas E. Peterson

The incidence of weed resistance to acetolactate synthase (ALS) inhibiting herbicides has increased in the United States. In 1993, a population of ALS-resistant common waterhemp was discovered after two confirmed applications of an imidazolinone herbicide. Following another imazethapyr application in the glasshouse, the resistant biotype demonstrated 130-fold resistance to imazethapyr at the whole plant level. The concentration of imazethapyr required to inhibit the ALS activity by 50% was 520 times greater for the resistant biotype than the susceptible. Plants also demonstrated cross-resistance to the sulfonylureas, chlorimuron and thifensulfuron, at the whole plant and enzyme levels. This particular discovery is of concern due to the low number of applications of the selection agent (imazaquin 1989, imazethapyr 1992, and imazethapyr in the greenhouse) and the high degree of cross-resistance eliminating several options for weed control.


2005 ◽  
Vol 83 (2) ◽  
pp. 99-109 ◽  
Author(s):  
D.S. Volenberg ◽  
D.E. Stoltenberg ◽  
C.M. Boerboom

Green foxtail (Setaria viridis) plants putatively resistant to acetolactate synthase (ALS) inhibitors were identified in a Wisconsin USA no-tillage soybean (Glycine max) field in 1999. Resistance to imidazolinone and sulfonylurea herbicides was characterized at the whole-plant level and enzyme level. Three- to four-leaf stage green foxtail plants were 1020, 53, and 6.5-fold resistant to imazethapyr, imazamox, and nicosulfuron, respectively, compared to susceptible plants. In vivo ALS was 1300 and 1.7-fold resistant to imazethapyr and nicosulfuron, respectively. These results suggested that this green foxtail accession was highly resistant to imazethapyr and imazamox, and that resistance was associated with an insensitive ALS enzyme.


Weed Science ◽  
2011 ◽  
Vol 59 (3) ◽  
pp. 431-437 ◽  
Author(s):  
Suphannika Intanon ◽  
Alejandro Perez-Jones ◽  
Andrew G. Hulting ◽  
Carol A. Mallory-Smith

Mayweed chamomile seeds were collected from six different fields across the Pacific Northwest. All populations (each collection site was considered a population) were suspected to have some level of acetolactate synthase (ALS) resistance. Greenhouse and laboratory studies were conducted to determine if these populations were resistant to three different classes of ALS inhibitors: sulfonylureas (SU), imidazolinones (IMI), and triazolopyrimidines (TP). A whole-plant dose–response andin vitroALS activity studies confirmed cross-resistance to thifensulfuron + tribenuron/chlorsulfuron (SU), imazethapyr (IMI), and cloransulam (TP); however, resistance varied by herbicide class and population. TwoALSisoforms of theALSgene (ALS1andALS2) were identified in mayweed chamomile; however, only mutations inALS1were responsible for resistance. No mutations were found inALS2. Sequence analysis of the partialALSgene identified four point mutations at position 197 (Pro197to Leu, Gln, Thr, or Ser) in the resistant populations. This study demonstrates genotypic variation associated with cross-resistance to ALS inhibitors within and between populations.


1999 ◽  
Vol 13 (1) ◽  
pp. 54-58 ◽  
Author(s):  
Christy L. Sprague ◽  
Amy L. Frasier ◽  
Donald Penner

Control of two perennial weeds, quackgrass and Canada thistle, and the differential sensitivities of three imidazolinone-resistant (IMI) corn hybrids and their sensitive isolines to various acetolactate synthase (ALS)-inhibiting herbicides were evaluated in greenhouse studies. The postemergence sulfonylurea herbicides nicosulfuron and primisulfuron controlled quackgrass > 80%. The imidazolinone herbicides imazapyr and imazamox applied postemergence controlled quackgrass 70 and 74%, respectively. Canada thistle control was 89% with the sulfonylurea herbicide metsulfuron. Primisulfuron, chlorsulfuron, and tribenuron controlled Canada thistle > 70%. The imidazolinonesensitive corn hybrids did not tolerate the imidazolinone herbicides imazethapyr, imazaquin, imazapyr, AC 263,222, and imazamox; the sulfonylurea herbicides chlorimuron, chlorsulfuron, metsulfuron, tribenuron, and triflusulfuron; and the pyrimidinylthiobenzoate herbicide pyrithiobac applied postemergence. The ‘Ciba 4393 IMR’ corn hybrid, homozygous for an unknown allele, was resistant to all of the various ALS-inhibiting herbicides that injured its sensitive isoline. The magnitude of resistance for this hybrid was greater than the other IR corn hybrids. The ‘Pioneer 3751 IR’ corn hybrid, homozygous for theXA-17ALS allele, was also resistant to a number of ALS-inhibiting herbicides. The ‘ICI 8692 IT’ corn hybrid, heterozygous for theMut2allele, was only resistant to the imidazolinone herbicides.


2012 ◽  
Vol 26 (3) ◽  
pp. 570-574 ◽  
Author(s):  
Hugh J. Beckie ◽  
Eric N. Johnson ◽  
Anne Légère

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.


1990 ◽  
Vol 4 (1) ◽  
pp. 169-172 ◽  
Author(s):  
Michael M. Primiani ◽  
Josephine C. Cotterman ◽  
Leonard L. Saari

A biotype of kochia resistant to chlorsulfuron has been isolated from a Kansas wheat field that had been treated with chlorsulfuron for five consecutive years. In greenhouse tests, the biotype also was resistant to both preemergence and postemergence herbicides with the same mode of action including imazapyr, CGA-131036, the methyl ester of metsulfuron, DPX-M6316, DPX-L5300, and the methyl ester of sulfometuron. The degree of cross resistance varied among the herbicides tested. Herbicides with different modes of action, including atrazine, bromoxynil, MCPA, and diuron, effectively controlled the resistant biotype in the greenhouse.


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