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Quantitative Trait Loci Mapping of Genome Regions Controlling Permethrin Resistance in the Mosquito Aedes aegypti

Saavedra-Rodriguez, K., Strode, Clare, Suarez, A. F., Salas, I. F., Ranson, Hilary ORCID: https://orcid.org/0000-0003-2332-8247, Hemingway, Janet ORCID: https://orcid.org/0000-0002-3200-7173 and Black, W. C. (2008) 'Quantitative Trait Loci Mapping of Genome Regions Controlling Permethrin Resistance in the Mosquito Aedes aegypti'. Genetics, Vol 180, Issue 2, pp. 1137-1152.

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Abstract

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 F, advanced intercross line. Parents came from a collection of mosquitoes from Isla Mrjeres, Mexico, that had been selected for permethrin resistance for two generations and a reference permethrin-susceptible strain originally from New Orleans. Following a 1-hr permethin exposure, 439 F-3 adult mosquitoes were phenotyped as knockdown resistant, knocked down/recovered, or dead. For QTL mapping, single nucleotide polymorphisms (SNPs) were identified at 22 loci with potential antixenobiotic activity including genes encoding cytochrome P450s (CYP), esterases (EST), or glutathione transferases (GST) and at 12 previously mapped loci. Seven antixenobiotic genes mapped to chromosome 1, 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 parasodium channel gene and the second with the CCEunk70 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.

Item Type: Article
Uncontrolled Keywords: insecticide resistance malaria vector pyrethroid resistance gene amplification anopheles-gambiae selection cuba microarray tolerance culicidae
Subjects: WC Communicable Diseases > Tropical and Parasitic Diseases > WC 750 Malaria
QX Parasitology > Insects. Other Parasites > QX 650 Insect vectors
QU Biochemistry > Genetics > QU 475 Genetic processes
QU Biochemistry > Genetics > QU 470 Genetic structures
WA Public Health > Preventive Medicine > WA 110 Prevention and control of communicable diseases. Transmission of infectious diseases
WA Public Health > Preventive Medicine > WA 240 Disinfection. Disinfestation. Pesticides (including diseases caused by)
WC Communicable Diseases > Tropical and Parasitic Diseases > WC 765 Prevention and control
QX Parasitology > Insects. Other Parasites > QX 510 Mosquitoes
QX Parasitology > Insects. Other Parasites > QX 600 Insect control. Tick control
QX Parasitology > Insects. Other Parasites > QX 525 Aedes
Faculty: Department: Groups (2002 - 2012) > Vector Group
Digital Object Identifer (DOI): https://doi.org/10.1534/genetics.108.087924
Depositing User: Users 183 not found.
Date Deposited: 05 Jul 2010 13:36
Last Modified: 09 Aug 2017 01:02
URI: https://archive.lstmed.ac.uk/id/eprint/907

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