High level methoprene resistance in the mosquito Ochlerotatus nigromaculis (Ludlow) in Central California
Abstract: In the summer of 1998, failures of methoprene field applications to control the mosquito Ochlerotatus nigromaculis (Ludlow) were noticed in several pastures in the outskirts of Fresno, Calif. Susceptibility tests indicated that the Fresno Oc nigromaculis populations had developed several thousand-fold higher LC50 and LC90 tolerance levels to methoprene compared with trithioate and 3-octylthio-1,1,1-trifluoro-2-propanone had little synergistic effect, suggesting that the mechanism of methoprene tolerance was not mediated by P450 mono oxygenese or carboxylesterase enzyme degradation. As part of initiating a resistance management strategy, partial reversion back to methoprene susceptibility was achieved in a resistant population after six consecutive applications of Bacillus thuringiensis israelensis Goldberg & Marga coupled with two oil and two pyrethrum+PBO applications.
Quantitative Trait Loci for Refractoriness of Anopheles gambiae to Plasmodium cynomolgi B
The severity of the malaria pandemic in the tropics is aggravated by the ongoing spread of parasite resistance to antimalarial drugs and mosquito resistance to insecticides. A strain of Anopheles gambiae, normally a major vector for human malaria in Africa, can encapsulate and kill the malaria parasites within a melanin-rich capsule in the mosquito midgut. Genetic mapping revealed one major and two minor quantitative trait loci (QTLs) for this encapsulation reaction. Understanding such antiparasite mechanisms in mosquitoes may lead to new strategies for malaria control.
Transient Expression of the Drosophilia melanogaster cinnabar Gene Rescues Eye Color in the White Eye (WE) Strain of Aedes Aegypti
The lack of eye pigment in the Aedes aegypti WE (white eye) colony was confirmed to be due to a mutation of the kynurenin hydroxylase gene, which catalyzes one of the steps in the metabolic synthesis of ommochrome eye pigments. Partial restoration of eye color (orange to red phenotype) in pupae and adults occurred in both sexes when first or second instar larvae were reared in water containing 3-hydroxykynurenin, the metabolic product of the enzyme kynurenin hydroxylase. No eye color restoration was observed when larvae were reared in water containing kynurenine sulfate, the precurser of 3-hydroxykynurenine in the ommochrome synthesis pathway. In addition, a plasmid clone containing the wild type Drosophila melanogaster gene encoding kynurenine hydroxylase, cinnabar (cn), was also able to complement the kynurenine hydroxylase mutation when it was injected into embryos of the A. aegypti WE strain. The ability to complement this A. aegypti mutant with the transiently expressed D. melanogaster cinnabar gene supports the value of this gene as a transformation reporter for use with A. aegypti WE and possibly other Diptera with null mutations in the kynurenine hydroxylase gene.