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Transcription of detoxification genes after permethrin selection in the mosquito Aedes aegypti
Author(s) -
SaavedraRodriguez K.,
Suarez A. F.,
Salas I. F.,
Strode C.,
Ranson H.,
Hemingway J.,
Black IV W. C.
Publication year - 2012
Publication title -
insect molecular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.955
H-Index - 93
eISSN - 1365-2583
pISSN - 0962-1075
DOI - 10.1111/j.1365-2583.2011.01113.x
Subject(s) - biology , aedes aegypti , gene , permethrin , genetics , gene knockdown , knockdown resistance , pesticide , botany , ecology , cyfluthrin , larva
Changes in gene expression before, during and after five generations of permethrin laboratory selection were monitored in six strains of Aedes aegypti : five F 2 – F 3 collections from the Yucatán Peninsula of Mexico and one F 2 from Iquitos, Peru. Three biological replicate lines were generated for each strain. The response to selection was measured as changes in the lethal and knockdown permethrin concentrations (LC 50 , KC 50 ) and in the frequency of the Ile1,016 substitution in the voltage‐gated sodium channel ( para ) gene. Changes in expression of 290 metabolic detoxification genes were measured using the ‘ Aedes Detox ’ microarray. Selection simultaneously increased the LC 50 , KC 50 and Ile1,016 frequency. There was an inverse relationship between Ile1,016 frequency and the numbers of differentially transcribed genes. The Iquitos strain lacked the Ile1,016 allele and 51 genes were differentially transcribed after selection as compared with 10–18 genes in the Mexican strains. Very few of the same genes were differentially transcribed among field strains but 10 cytochrome P 450 genes were upregulated in more than one strain. Laboratory adaptation to permethrin in Ae. aegypti is genetically complex and largely conditioned by geographic origin and pre‐existing target site insensitivity in the para gene. The lack of uniformity in the genes that responded to artificial selection as well as differences in the direction of their responses challenges the assumption that one or a few genes control permethrin metabolic resistance. Attempts to identify one or a few metabolic genes that are predictably associated with permethrin adaptation may be futile.