A triazine-resistant (TR) biotype of Powell amaranth was discovered in 1989 in a potato field treated with metribuzin. A survey of all agricultural counties in Idaho showed that the TR Powell amaranth infestation was localized in the southeastern corner of Gooding county in southern Idaho. To determine the mechanism of triazine resistance, I50 values for inhibition of photosystem II were determined for atrazine, metribuzin, and diuron using thylakoids isolated from TR and triazine-susceptible (TS) biotypes. TR/TS ratios based on I50 values were 134 for atrazine, 62 for metribuzin, and 1.9 for diuron. Results of binding studies with atrazine and metribuzin were consistent with the I50 studies, indicating that resistance was due to reduced binding of triazines to the thylakoid membrane D1 protein. Sequencing the chloroplast psbA gene from TR and TS biotypes revealed a serine 264 to glycine change in the TR biotype. The mutation presumably resulted in reduced hydrogen bonding between triazine herbicides and the Dl protein.
