- THIS ARTICLE
- Full Text (Rapid PDF)
-
All Versions of this Article:
genetics.108.087924v1
genetics.108.087924v2
180/2/1137 most recent - Alert me when this article is cited
- Alert me if a correction is posted
- SERVICES
- Similar articles in this journal
- Similar articles in PubMed
- Alert me to new issues of the journal
- Download to citation manager
- Reprints & Permissions
- GOOGLE SCHOLAR
- Articles by Saavedra-Rodriguez, K. L.
- Articles by Black, W. C.
- PUBMED
- PubMed Citation
- Articles by Saavedra-Rodriguez, K. L.
- Articles by Black, W. C.
doi:10.1534/genetics.108.087924
A more recent version of this article appeared on October 1, 2008.
REGULAR RESEARCH PAPERS |
QTL mapping of genome regions controlling permethrin resistance in the mosquito Aedes aegypti
Karla Lizet Saavedra-Rodriguez 1, Clare Strode 2, Adriana Flores Suarez 3, Ildefonso Fernandez Salas 3, Hilary Ranson 2, Janet Hemingway 2 and William Cormack Black 1*
1 Colorado State University
2 Liverpool School of Tropical Medicine
3 Universidad Autonoma de Nuevo Leon
* To whom correspondence should be addressed. E-mail: wcb4{at}lamar.colostate.edu.
Submitted on February 11, 2008
Revised on April 1, 2008
Accepted on 7 July 2008
The mosquito Aedes aegypti is the principal vector of dengue and yellow fever flaviviruses. Permethrin is an insecticide used to suppress Ae. aegypti adult populations but metabolic and target site resistance to pyrethroids has evolved in many locations worldwide. Quantitative Trait Loci (QTL) controlling permethrin survival in Ae. aegypti were mapped in an F3 advanced intercross line. Parents came from a collection of mosquitoes from Islas Mujeres, Mexico that had been selected for permethrin resistance for two generations and a reference permethrin-susceptible strain originally from New Orleans. Following a 1 hour permethrin exposure, 439 F3 adult mosquitoes were phenotyped as either knock down resistant, knocked down/recovered or dead. For QTL mapping, single nucleotide polymorphisms (SNPs) were identified at 22 loci with potential anti-xenobiotic activity including genes encoding cytochrome P450s (CYP), esterases (EST) or glutathione transferases (GST) and at 12 previously mapped loci. Seven anti-xenobiotic genes mapped to chromosome I, six to chromosome II and nine to chromosome III. Two QTL of major effect were detected on chromosome III. One corresponds with a SNP previously associated with permethrin resistance in the para sodium channel gene and the second with the CCEunk7o esterase marker. Additional QTL but of relatively minor effect were also found. These included two sex linked QTL on chromosome I affecting knockdown and recovery, and a QTL affecting survival and recovery. On chromosome II, one QTL affecting survival and a second affecting recovery were detected. The patterns confirm that mutations in the para gene cause target site insensitivity and are the major source of permethrin resistance but that other genes dispersed throughout the genome contribute to recovery and survival of mosquitoes following permethrin exposure.
Key Words: Aedes aegypti, Linkage mapping, QTL mapping, insecticide resistance, knockdown resistance