A - Papers appearing in refereed journals
Cocker, K. M., Moss, S. R. and Coleman, J. O. D. 1999. Multiple mechanisms of resistance to fenoxaprop-P -ethyl in United Kingdom and other European populations of herbicide- resistant Alopecurus myosuroides (black-grass). Pesticide Biochemistry and Physiology. 65 (3), pp. 169-180.
|Authors||Cocker, K. M., Moss, S. R. and Coleman, J. O. D.|
This study investigated the biochemical mechanisms that bestow resistance to fenoxaprop-P-ethyl in a range of European field populations of the grass weed black-grass (Alopecurus myosuroides). Eleven populations were assessed for resistance to fenoxaprop-P-ethyl in a glasshouse experiment. Results confirmed that two populations (Roth and Lars) were susceptible and that the remaining nine populations showed different degrees of resistance to fenoxaprop-P-ethyl. Biochemical analysis of fenoxaprop-P-ethyl metabolism and target site sensitivity showed that, although enhanced metabolism played an important role in herbicide resistance in black-grass, it could not account for resistance in all of the populations. Resistance at the whole-plant level correlated well with reduced acetyl Co-enzyme A carboxylase sensitivity (target site resistance) in two of the populations (one from the United Kingdom and one from Germany) but enhanced metabolism appeared to be the primary mechanism of resistance in the majority of the other populations. The greatest level of enhanced metabolism occurred in the population from Belgium. We suggest that resistance in Lincs E1 may be explained by multiple resistance mechanisms—the expression of both insensitive acetyl Co-enzyme A carboxylase and an increased rate of detoxification. However, resistance in the population Clay from the United Kingdom could be explained neither by target site insensitivity nor by an enhanced rate of metabolism. These results provide conclusive evidence that a single resistance mechanism alone cannot explain insensitivity to fenoxaprop-P-ethyl in European resistant black-grass populations and that additional, as yet uncharacterized, mechanisms must also be present.
|Year of Publication||1999|
|Journal||Pesticide Biochemistry and Physiology|
|Journal citation||65 (3), pp. 169-180|
|Digital Object Identifier (DOI)||doi:10.1006/pest.1999.2439|
|Open access||Published as non-open access|
|Funder project or code||202|
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