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Independent mutations in the Rdl locus confer dieldrin resistance to Anopheles gambiae and An. arabiensis
Author(s) -
Du W.,
Awolola T. S.,
Howell P.,
Koekemoer L. L.,
Brooke B. D.,
Benedict M. Q.,
Coetzee M.,
Zheng L.
Publication year - 2005
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.1365-2583.2005.00544.x
Subject(s) - anopheles gambiae , biology , dieldrin , genetics , locus (genetics) , avermectin , serine , allele , alanine , asparagine , glycine , gene , biochemistry , amino acid , malaria , pesticide , ecology , phosphorylation , anatomy , immunology
Substitutions of a conserved alanine residue in the Rdl locus coding for a γ‐aminobutyric acid (GABA) receptor subunit with serine or glycine confer resistance to dieldrin in various insect species. Here, we show that alanine to glycine substitution in the Rdl locus of the malaria vector, Anopheles gambiae , is genetically linked to resistance to dieldrin. An alanine to serine substitution developed independently in a dieldrin resistant strain of An. arabiensis . An allele‐specific polymerase chain reaction (PCR) assay was able to differentiate dieldrin resistant and susceptible mosquitoes.