Palmer amaranth (Amaranthus palmeri) is a major weed in corn (Zea mays) fields in the southern Great Plains of the United States. Field studies were conducted in 1996, 1997, and 1998 near Garden City, KS, to evaluate the effects of Palmer amaranth density and time of emergence on grain yield of irrigated corn and on seed production of Palmer amaranth. Palmer amaranth was established at densities of 0.5, 1, 2, 4, and 8 plants m−1 of corn row both concurrently at corn planting and when corn was at the three- to six-leaf stage. The control plots were weed free. The Palmer amaranth planted with corn emerged with corn, whereas that planted later emerged at the four-, six-, and seven-leaf stages of corn. The Palmer amaranth emerging with corn reduced yield from 11 to 91% as density increased from 0.5 to 8 plants m−1 of row. In contrast, yield loss from Palmer amaranth emerging later than corn was observed only when the emergence occurred at the four- and six-leaf stages. The corn leaf area index (LAI) decreased as Palmer amaranth density increased. Reduction in corn LAI from Palmer amaranth interference was smaller for the second emergence date than for the first emergence date. Seed production per Palmer amaranth plant decreased with greater density, but seed per unit area increased from 140,000 to 514,000 seeds m−2 at densities of 0.5 and 8 plants m−1 of row, respectively, when Palmer amaranth emerged with corn and from 1,800 to 91,000 seeds m−2 at the same densities for later emergence dates. Although Palmer amaranth is highly competitive in corn, this study shows that yield loss is affected more by time of emergence than by density.

Resistance to imazethapyr was identified in a population of common sunflower that had been treated with imazethapyr for seven consecutive years. The imazethapyr-resistant biotype of common sunflower was approximately 170 times more resistant to imazethapyr than the susceptible biotype based on the rate required for 25% control. Resistance was due to altered acetolactate synthase (ALS) that is less sensitive to imazethapyr. The imazethapyr concentration required to inhibit in vitro ALS activity by 25% was 210–fold higher in the resistant biotype than in the susceptible biotype. Differences in absorption, translocation, and metabolism of imazethapyr in common sunflower biotypes were not sufficient to explain the resistance to imazethapyr.

We confirm the first case of evolution of resistance to four herbicide sites of action (PSII, ALS and EPSPS inhibitors and synthetic auxins) in a single kochia population, and target-site-based mechanisms confer resistance to atrazine, glyphosate and chlorsulfuron.