Independent mutations in the Rdl locus confer dieldrin resistance to Anopheles gambiae and An. arabiensis.
Substitutions of a conserved alanine residue in the Rdl locus coding for a gamma-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.
Du
W
W
Yale University School of Medicine, Epidemiology and Public Health, New Haven, CT 06520, USA.
Awolola
T S
TS
Howell
P
P
Koekemoer
L L
LL
Brooke
B D
BD
Benedict
M Q
MQ
Coetzee
M
M
Zheng
L
L
D000595:Amino Acid Sequence; D000818:Animals; D000852:Anopheles / Q000235:genetics / Q000378:metabolism*; D001483:Base Sequence; D017931:DNA Primers; D004026:Dieldrin; D007305:Insecticide Resistance / Q000235:genetics*; D008969:Molecular Sequence Data; D009154:Mutation / Q000235:genetics*; D016133:Polymerase Chain Reaction / Q000379:methods; D011963:Receptors, GABA-A / Q000235:genetics*; D016415:Sequence Alignment; D017422:Sequence Analysis, DNA; D013045:Species Specificity
D017931:DNA Primers; D011963:Receptors, GABA-A; D004026:Dieldrin