The crop-weed interference relationship is a critical component of bioeconomic weed management models. Multi-year field experiments were conducted at five locations to determine the stability of corn-velvetleaf interference relationships across years and locations. Two coefficients (I and A) of a hyperbolic equation were estimated for each data set using nonlinear regression procedures. The I and A coefficients represent percent corn yield loss as velvetleaf density approaches zero, and maximum percent corn yield loss, respectively. The coefficient I was stable across years at two locations, but varied across years at one location. The coefficient A did not vary across years within locations. Both coefficients, however, varied among locations. Results do not support the use of common coefficient estimates for all locations within a region.
Glyphosate is a nonselective herbicide used as a harvest aid in a variety of crops. Glyphosate is absorbed into the foliage and translocated to metabolically active regions in the plant where it interferes with the shikimic acid pathway. Experiments were conducted to determine the accumulation and distribution of shikimic acid in wheat treated with glyphosate at soft and hard dough stages of kernel development and to determine the fate of shikimic acid during milling and bread making. Elevated levels of shikimic acid were detected throughout the wheat plant. Shikimic acid concentrations peaked 3-7 days after treatment and then declined until harvest. Shikimic acid content was 3-fold greater in flour and 2-fold greater in the bread derived from treated wheat than nontreated wheat. Similarly, elevated levels of shikimic acid were found in the crumbs and crust of bread made with flour from glyphosate treated wheat. Glyphosate applied preharvest resulted in shikimic acid accumulation in hard red spring wheat and subsequent end-use products.
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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