1996
DOI: 10.1006/pest.1996.0070
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Triallate Resistance inAvena fatuaL. Is Due to Reduced Herbicide Activation

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Cited by 32 publications
(33 citation statements)
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“…Similarly, the high‐level antagonism between prosulfocarb or triallate and phorate confirms that in vivo bioactivation of these thiocarbamate pro ‐herbicides is necessary to cause phytotoxic herbicide damage, but also suggests possible metabolism‐based resistance mechanism(s) for these two thiocarbamate herbicides. For example, in Avena fatua , reduced herbicide metabolic activation via sulfoxidation was found to mediate triallate resistance …”
Section: Discussionmentioning
confidence: 99%
“…Similarly, the high‐level antagonism between prosulfocarb or triallate and phorate confirms that in vivo bioactivation of these thiocarbamate pro ‐herbicides is necessary to cause phytotoxic herbicide damage, but also suggests possible metabolism‐based resistance mechanism(s) for these two thiocarbamate herbicides. For example, in Avena fatua , reduced herbicide metabolic activation via sulfoxidation was found to mediate triallate resistance …”
Section: Discussionmentioning
confidence: 99%
“…Thus, P450‐mediated enhanced herbicide degradation was hypothesised as the mechanism conferring resistance by higher herbicide detoxification ability, as also demonstrated in another study with the same population resistant to a different herbicide mode of action . Conversely, in A. fatua , reduced herbicide activation via a much slower rate of herbicide sulfoxidation (probably P450 mediated) appeared to be the mechanism of resistance to triallate . In addition, a greater level of endogenous giberellin in triallate‐resistant plants could contribute to resistance during early developmental stages of seedlings .…”
Section: Discussionmentioning
confidence: 99%
“…Experimental evidence seems to suggest some diversity of mechanisms in response to triallate in different Avena populations . As most thiocarbamates need in vivo sulfoxidation to deliver herbicidal activity, it has been suggested that a differential rate of herbicide metabolism and subsequent reduced herbicide activation mediate levels of resistance to triallate in A. fatua populations . In addition, studies revealed a potential involvement of endogenous giberellin in resistant populations, with greater gibberellin levels in resistant populations that could result in rapid meristematic growth and preclude phytotoxic levels of thiocarbamate herbicides from reaching the shoot meristem during the most sensitive plant developmental stages …”
Section: Three Major Cases Of Herbicide‐resistant Weeds In Three Cropmentioning
confidence: 99%
“…Thus, currently there is the opportunity to control wild oat by selecting from a diverse range of herbicide modes of action, acting at different stages of crop growth (preseeding, seeding, post-seeding, and late stem elongation). However, there should not be complacency, as previous work has identified Avena populations that have developed resistance to ALS-inhibiting herbicides (Beckie et al 1999;Mengistu et al 2003), triallate (Kern et al 1996), and flamprop-methyl (Friesen et al 2000;Broster 2004). Nevertheless, the availability of herbicide diversity means that herbicide resistance evolution in wild oat can be minimised through diverse herbicide usage and rotation, together with cultural management practices.…”
Section: Future Implicationsmentioning
confidence: 99%