A seedling bioassay was used to determine the response of triallate-resistant (R) and -susceptible (S) wild oat populations to difenzoquat and EPTC. The bioassay, based on seedling shoot length at 10 d after treatment, provided a reliable and rapid means of determining if wild oat populations were resistant to difenzoquat. Using a bioassay concentration of 15 ppm difenzoquat, it was possible to identify populations that were resistant to the recommended foliar-applied rate (0.85 kg ai/ha). Expected herbicide dosages that reduced shoot length by 50% (ED50) derived from nonlinear regression analysis indicated three and two levels of response to difenzoquat among eight S and seven R populations, respectively, indicating within population variability in their response to difenzoquat. Of the populations tested, none was resistant to EPTC. On the contrary, some R populations had lower ED50 values than did S populations, suggesting an increased sensitivity to EPTC.

Resistance to bromoxynil and terbacil was confirmed in common groundsel collected from peppermint (Mentha piperita) fields in Oregon. This is the first reported case of a bromoxynil-resistant weed selected under field conditions. The bromoxynil rate required to reduce growth by 50% was 10 times higher for the resistant biotype than for the susceptible biotype. The bromoxynil-resistant biotype also was resistant to terbacil.

Following six consecutive annual applications of imazaquin in combination with trifluralin or pendimethalin to several soybean fields on the Delmarva Peninsula, unacceptable smooth pigweed control was observed. Field and greenhouse studies were conducted to determine if this population of smooth pigweed was resistant to imazaquin and other herbicides. In field research, imazaquin and imazethapyr gave complete control of the susceptible (S) population while providing no control of the resistant (R) population; pyrithiobac controlled 99 and 90% of the R and S populations, respectively. Pendimethalin, metribuzin, MON-12000, and flumiclorac gave less than 75% control of both S and R populations. Chlorimuron, primisulfuron, CGA-152005, and lactofen gave above 75% control, and thifensulfuron and nicosulfuron gave above 90% control of both S and R populations. Seeds were collected from the R and S smooth pigweed populations for research in the greenhouse. Greenhouse studies confirmed high levels of resistance to imazaquin and imazethapyr and low levels of cross-resistance to rimsulfuron and chlorimuron in the R population. Susceptibility of the R population to nicosulfuron, thifensulfuron, pyrithiobac, and pendimethalin was comparable to that of the S population.

The study was conducted to determine the cross-resistance of imazethapyr-resistant common sunflower (Helianthus annuus) to selected imidazolinone, sulfonylurea, and triazolopyrimidine herbicides. Whole-plant herbicide dose–response curves and in vitro enzyme studies showed that imazethapyr-resistant common sunflower was highly resistant to imazamox, slightly resistant to thifensulfuron and chlorimuron, and not resistant to cloransulam. Resistance ratios of herbicide concentrations required to inhibit growth by 25% were 310, 3.3, 2.0, and 1.4 times greater in the resistant biotype than in the susceptible biotype for imazamox, thifensulfuron, chlorimuron, and cloransulam, respectively. Similarly, herbicide concentrations required to inhibit ALS activity in vitro by 25% were 332.0, 18.6, 8.3, and 1.2 times greater in the resistant biotype than in the sensitive biotype for imazamox, chlorimuron, thifensulfuron, and cloransulam, respectively.

Greenhouse and field experiments were conducted to confirm and quantify linuron resistance in common purslane (Portulaca oleracea) collected from a carrot (Daucus carota) field in Imlay City, MI. Preliminary evaluation was made using a flotation test kit to identify resistance to linuron and atrazine. Subsequent greenhouse experiments indicated that this common purslane was resistant to 11.2 kg/ha linuron and 179 kg/ha atrazine. The resistance ratio for linuron was > 300 and was > 400 for atrazine. The resistant common purslane was also highly resistant to diuron, cyanazine, and prometryn but had a low level of negative cross-resistance to bromoxynil. Both resistant and susceptible biotypes of common purslane were sensitive to hexazinone and bentazon.

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.

Biotypes of smallflower umbrella sedge and ricefield bulrush resistant to acetolactate synthase (ALS)-inhibiting herbicides have been reported in several rice areas of the world. Here, we present results of a study conducted on whole plants of seven smallflower umbrella sedge and four ricefield bulrush biotypes collected in Italian, Spanish, and Californian rice fields to evaluate cross-resistance to ALS herbicides in these important weeds of temperate rice. The following herbicides were tested: bensulfuron-methyl, halosulfuron, cinosulfuron, imazamox, and bispyribac-sodium. The smallflower umbrella sedge and ricefield bulrush biotypes studied exhibited different cross-resistance patterns, some of which have not been previously reported. The Italian smallflower umbrella sedge biotype was cross-resistant to bensulfuron-methyl, cinosulfuron, imazamox, and bispyribac-sodium, but was susceptible to halosulfuron. One smallflower umbrella sedge biotype from California was also resistant to bensulfuron-methyl, imazamox, and bispyribac-sodium, but had a lower level of resistance to halosulfuron. In contrast, the second smallflower umbrella sedge biotype from California was strongly resistant to halosulfuron and was also resistant to bensulfuron-methyl and bispyribac-sodium, but moderately resistant to imazamox. The Spanish smallflower biotype was resistant to the sulfonylurea herbicides bensulfuron-methyl and halosulfuron. Different responses were observed in ricefield bulrush. The Italian biotype was resistant to the sulfonylureas only, whereas the biotype from California exhibited broad cross-resistance to all the ALS herbicides tested. Knowledge on cross-resistance is needed to formulate herbicide use and weed management strategies for delaying the evolution of resistance to ALS herbicides in rice systems.

Littleseed canarygrass, a troublesome wheat weed, has developed resistance against isoproturon in India. Laboratory, pot, and field experiments were conducted to quantify the level of isoproturon resistance in various littleseed canarygrass biotypes and to evaluate the response of isoproturon-resistant littleseed canarygrass to alternate herbicides. For quantification of resistance, 10 littleseed canarygrass biotypes were collected from fields with a varied history of cropping and herbicide use. Pot studies indicated that 6 out of the 10 biotypes tested were resistant to isoproturon. The resistant (R) biotypes had 50% growth reduction values, 5 to 10 times greater than that of the most susceptible biotype. The R biotypes were from areas where isoproturon had been used continuously for more than 10 yr in wheat under a continuous rice–wheat cropping system. The isoproturon resistance was not detected where crops and herbicides were rotated. Under field conditions, postemergence isoproturon at 1,000 g/ha 32 d after sowing failed to control littleseed canarygrass and as a result wheat grain yield decreased by 65% compared with the weed-free control. The herbicides observed to be effective in wheat against isoproturon-resistant littleseed canarygrass were CGA 184927 (50 to 60 g ai/ha), fenoxaprop-p-ethyl (100 to 120 g/ha), ICIA 0604 (350 g ai/ha), and MON 37503 (25 g ai/ha). The use of these herbicides increased the grain yield by 200% or more when compared with the weedy check. Among the herbicides tested, MON 37503 at 25 g ai/ha was the best because of complex weed flora control and produced wheat yield similar to that of the weed-free control. Based on this study, the absence of resistance when herbicides and crops were rotated indicates that growers should follow herbicide and crop rotation in order to avoid development of herbicide resistance in the near future. The integration of this system (crop and herbicide rotation) with cultural and mechanical means of weed control could be further targeted as a long-term strategy for resistance management.

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.

Of 78 biotypes of wild radish (Raphanus raphanistrum) collected from Western Australia (WA), 42% were resistant and 14% intermediate to acetolactate synthase (ALS)-inhibiting herbicides. Based on the LD50 and GR50 ratios, the resistant biotype K96071 was 81-fold more resistant to chlorsulfuron and 114- to 116-fold more resistant to metosulam than the susceptible biotype K96041. More resistant biotypes were found in northern zones than in southern zones of WA. Resistant biotypes evolved after five applications of chlorsulfuron in a predominantly cereal–lupin rotation. Where resistant biotypes were found, ALS-inhibiting herbicides were not rotated with herbicides with different modes of action as frequently as in fields with susceptible biotypes. Cross-resistance to chlorsulfuron and metosulam was found in the resistant biotypes even though only 15% of the 78 biotypes were exposed to two applications of metosulam over a 10-yr period. All 78 biotypes were effectively controlled by simazine and 2,4-D amine.

Diagnosing herbicide-resistant weeds as a first step in resistance management and monitoring their nature, distribution, and abundance demands efficient and effective screening tests. This review summarizes and recommends appropriate seed sampling techniques, protocols for screening weeds for resistance to herbicides of different sites of action, interpretation of results, and information given to the grower. Elements common to all screening procedures are reviewed. Choosing appropriate discriminating doses to distinguish between resistant and susceptible weed biotypes is the most important factor in achieving accurate and consistent results. Interpretation of results is also critical because resistant weeds may comprise a small portion of the population in suspected accessions or biotypes.