A - Papers appearing in refereed journals
Devonshire, A. L., Field, L. M., Foster, S. P., Moores, G. D., Williamson, M. S. and Blackman, R. L. 1998. The evolution of insecticide resistance in the peach-potato aphid, Myzus persicae. Philosophical Transactions of the Royal Society B-Biological Sciences. 353 (1376), pp. 1677-1684.
|Authors||Devonshire, A. L., Field, L. M., Foster, S. P., Moores, G. D., Williamson, M. S. and Blackman, R. L.|
The peach–potato aphid Myzus persicae (Sulzer) can resist a wide range of insecticides, but until recently (1990) the only mechanism identified was the increased production of carboxylesterases (E4 or FE4), which cause enhanced degradation and sequestration of insecticidal esters. We have now identified two forms of target–site resistance involving changes in the acetylcholinesterase (AChE) and sodium channel (kdr) genes. Biochemical and DNA diagnostic methods can be used to identify all three mechanisms in individual aphids, and thereby establish their spatial distributions and temporal dynamics. Amplified genes underlie the increased production of esterases but their expression is modulated by DNA methylation. Amplification of the E4 gene is in strong linkage disequilibrium with the kdr mechanism. This may reflect strong insecticidal selection favouring aphids with multiple mechanisms, tight chromosomal linkage and/or the prominence of parthenogenesis in many M. persicae populations. The decreased fitness of resistant aphids under winter conditions may be a consequence of the altered sodium–channel gene affecting behaviour and/or the perception of external stimuli.
|Year of Publication||1998|
|Journal||Philosophical Transactions of the Royal Society B-Biological Sciences|
|Journal citation||353 (1376), pp. 1677-1684|
|Digital Object Identifier (DOI)||doi:10.1098/rstb.1998.0318|
|Open access||Published as non-open access|
|Funder project or code||235|
|Online||29 Oct 1998|
|Publisher||Royal Society Publishing|
|Royal Society Publishing|
|Copyright license||Publisher copyright|
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