Genetic mapping of two loci affecting DDT resistance in the malaria vectorAnopheles gambiae

Resistance to the insecticide DDT in the mosquito vectors of malaria has se verely hampered efforts to control this disease and has contributed to the increase in prevalence of malaria cases seen in recent years. Over 90% of t he 300-500 million annual cases of malaria occur in Africa, where the major vector is Anopheles gambiae. DDT resistance in the ZAN/U strain of An. gam biae is associated with an increased metabolism of the insecticide, catalys ed by members of the glutathione S-transferase (GST) enzyme family, but the molecular mechanism underlying this metabolic resistance is not known. Gen etic crosses show that resistance is autosomal and semidominant. We have us ed microsatellite markers to identify two quantitative trait loci (QTL), wh ich together explain over 50% of the variance in susceptibility to DDT in t he ZAN/U strain of An. gambiae. The first locus, rtd1, is on chromosome 3 b etween markers H341 and H88 and has a recessive effect with respect to susc eptibility. The second locus, rtd2 is on chromosome 2L, close to marker H32 5 and has an additive genetic effect. The markers flanking these two QTL ha ve been physically mapped to An. gambiae polytene chromosomes. They do not coincide with any of the GST genes that have been cloned and mapped in this species. Characterization of these QTL will lead to a clearer understandin g of the mechanisms of metabolic resistance to DDT.