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Summary A population of Bromus tectorum infesting an olive grove at Córdoba (Spain) survived simazine use rates of 3.0 kg a.i. ha−1 over two consecutive years. Non‐tillage olive monoculture and two annual simazine applications had been carried out for 10 years. The resistant biotype showed a higher ED50 value (7.3 kg a.i. ha−1) than that of the susceptible control (0.1 kg a.i. ha−1), a 73‐fold increase in herbicide tolerance. The use of fluorescence, Hill reaction, absorption, translocation and metabolism assays showed that simazine resistance in this biotype was caused by a modification of the herbicide target site, since chloroplasts from the resistant biotype of B. tectorum were more than 300 times less sensitive to simazine than those from the susceptible biotype. In addition, non‐treated resistant plants of B. tectorum displayed a significant reduction in the QA to QB electron transfer rate when compared with the susceptible biotype, a characteristic that has been linked to several mutations in the protein D1 conferring resistance to PS II inhibiting herbicides. Resistant plants showed cross‐resistance to other groups of triazine herbicides with the hierarchy of resistance level being methoxy‐s‐triazines ≥chloro‐s‐triazines > methylthio‐s‐triazines > cis‐triazines. The results indicate a naturally occurring target‐site point mutation is responsible for conferring resistance to triazine herbicides. This represents the first documented report of target site triazine resistance in this downy brome biotype.
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Menéndez et al. (2007) studied this question.
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