Characterization of an atrazine-resistant biotype of jimsonweed (Datura stramonium L.) from Indiana
Abstract
A jimsonweed biotype resistant to atrazine was discovered in southern Indiana in 1991. This was the first report of triazine resistance in jimsonweed worldwide. Experiments showed the resistant jimsonweed had a novel combination of mutations for triazine-resistant plants. It has a glycine and a lysine substitution at positions 264 and 238 of the D1 photosystem II protein, while most dicot plants have a serine and an arginine, respectively at these positions. Laboratory, greenhouse and field experiments with whole plants, leaf disks, chloroplasts and thylakoids of resistant and susceptible jimsonweed biotypes were conducted. They studied the effects of these mutations on photosynthetic capacity, plant growth, competitive ability, reproductive fitness and response to a variety of photosystem II inhibiting herbicides. Binding kinetics of atrazine to thylakoids of susceptible and resistant biotypes was also investigated. In our experiments atrazine-resistant jimsonweed was less competitive, had lower photosynthetic efficiency, produced fewer seeds and total plant biomass than atrazine-susceptible biotypes. These responses agree with those that have been commonly shown for all studied atrazine-resistant weed biotypes. However, our atrazine-resistant jimsonweed differs in several respects from other atrazine-resistant plants. Some atrazine does bind to the D1 protein of the resistant biotype, and this binding is correlated with injury in whole plants treated with this herbicide. The atrazine concentration necessary to inhibit photosynthesis in the resistant biotype was 50 fold greater than that required to inhibit photosynthesis in the susceptible biotype. This level of resistance is lower than that of all other triazine-resistant weeds. Unlike reported responses in other triazine resistant weeds, atrazine-resistant jimsonweed has a variable resistance to specific triazine herbicides, being susceptible to commercial rates of prometryn, while being extremely resistant to simazine ($>$465x fold). These findings suggest that the mutations in the herbicide binding protein responsible for atrazine resistance may also be responsible for the unexpected responses we observed and warrant further study.
Degree
Ph.D.
Advisors
Weller, Purdue University.
Subject Area
Botany|Botany|Range management
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