Abstract
In 1970, Ryan (Ryan, 1970) reported that a population of Senecio vulgaris (L.) was not controlled by recommended rates of simazine in a conifer nursery in Washington state (USA). Since this first report, resistance to photosystem II (PS II) inhibitor herbicides has become widespread. In terms of numbers of species, triazine resistance is the most prevalent type of herbicide resistance found in weeds (Holt and LeBaron, 1990; LeBaron, 1991; LeBaron and MacFarland, 1990). The most recent worldwide survey of herbicide resistance, which was conducted in 1989, indicated that there were 57 weed species with biotypes resistant to triazine herbicides (LeBaron, 1991). In the majority of cases, resistance to PS II-inhibiting herbicides is due to a modification at the target site, the DI protein of the PS II reaction center (Trebst, 1991). Since the mid-1980’s, there have been increasing reports of resistance to PS II inhibitors due to enhanced herbicide detoxification (Burnet et al., 1993a,b; Gronwald et al., 1989; Hoagland et al., this volume; Kemp et al., 1990; Leah et al., 1994).
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Gronwald, J.W. (1997). Resistance to PS II Inhibitor Herbicides. In: De Prado, R., Jorrín, J., García-Torres, L. (eds) Weed and Crop Resistance to Herbicides. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-5538-0_5
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