Field studies were conducted from 1997 to 1999 in Westminster, MD, to evaluate a variety of preemergence (PRE) and postemergence (POST) herbicide programs on crop injury and control of triazine-resistant common lambsquarters (TR-CHEAL) in no-till corn. In 1997 PRE studies, combinations of metolachlor with flumetsulam or halosulfuron and high rates of rimsulfuron + thifensulfuron (0.02 + 0.009 kg ai/ha) injured corn most 4 weeks after treatment (WAT), averaging 11 to 15%. In 1998 and 1999, metolachlor plus a high rate of halosulfuron (0.07 kg/ha) injured corn most 4 WAT, averaging 13 and 10%, respectively. High rates of rimsulfuron + thifensulfuron also provided a higher level of corn injury in 1998 and 1999 in comparison with many of the other treatments. However, for all three years of the study, no injury was observed from any PRE treatment 8 WAT. In 1997 and 1998, at 8 WAT, combinations of metolachlor with flumetsulam or halosulfuron provided greater TR-CHEAL control than many of the other treatments, averaging 98 and 100%, respectively. In 1999, however, control of TR-CHEAL with these same treatments did not vary in comparison with most of the other treatments. At 8 WAT, there was a trend for increased TR-CHEAL control as the rates of RPA-201772 and rimsulfuron + thifensulfuron increased. Control of TR-CHEAL with metolachlor + atrazine + pendimethalin varied across years 8 WAT. Similar observations were made 16 WAT. In 1997, POST applications of dicamba, SAN 1269H at 0.3 lb ai/ha, primisulfuron + dicamba, and primisulfuron + CGA 152005 + dicamba provided the highest level of TR-CHEAL control 8 WAT, averaging 93, 93, 95, and 93%, respectively. In 1998, with the exception of carfentrazone + atrazine, all POST treatments provided 90% control of TR-CHEAL or better 8 WAT. In 1999, POST applications of SAN 1269H at 0.3 kg/ha, pyridate + atrazine, and primisulfuron + CGA 152005 + pyridate provided the highest level of TR-CHEAL control, averaging 80, 90, and 96%, respectively, 8 WAT. With the exception of carfentrazone + atrazine, control of TR-CHEAL with the other POST treatments varied in 1999 from 60 to 74% 8 WAT. Carfentrazone + atrazine applied POST provided the lowest level of TR-CHEAL control 8 WAT averaging 28, 37, and 17% for 1997 to 1999, respectively.

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 of EPSPS revealed no target-site mutation at Thr102 or Pro106 residue. MHR kochia accessions had increased relative EPSPS gene 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 Pro197 amino acid substitution (proline to glutamine). EPSPS gene amplification and a single target-site mutation at Pro197 in ALS gene 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.