| The genetic linkage of CYP6B10, a gene which controls insecticide detoxication, and hscp, which encodes the sodium channel target of various insecticides, was investigated using backcross families of, tobacco budworm, Heliothis virescens, a pestiferous insect. Both genes have been implicated in resistance to insecticides. The genetic distance between these genes was less than 2.1 cM as estimated by the lack of recombination between them. This result suggests the possibility of a resistance cassette in this species and it could have serious implications for management of this pest.; The tobacco budworm is an important economic pest of agricultural crops. Pyrethroid insecticides were applied frequently to control this pest; however, pyrethroid resistance has increased gradually limiting the use of the older, less toxic pyrethroid analogs. The Bt (Bacillus thuringiensis) toxin is a very powerful insecticide engineered into crop plants to control this pest. Even though Bt resistance has not been observed in the field strains, several resistance genes were observed experimentally in laboratory colonies. Understanding of the resistance mechanism is necessary to avoid resistance and to control the insect in the long term.; A genomic approach is useful in the studies of mechanisms of insecticide resistance. Linkage mapping is one of the methods to analyze multiple resistance mechanisms. Linkage analysis of H. virescens has been studied; however, few genes were published and there was little or no information on visible markers or easy to score single nucleotide polymorphisms (SNPs).; Linkage relationships were determined among several genes for pigmentation as visible markers and among several SNPs including some with relevance to insecticide mode of action. In test crosses with visible markers, the independent assortment of y with ye and y with yes was observed (the y gene controlled yellow scales, the ye gene controlled greenish-yellow eyes, and the yes gene controlled yellow scales and yellow eyes).; SNPs were discovered in CYP6B10, IIS6 of hscp (helothis sodium channel protein), Hpy of hscp, TPI, JHE, and Cry1 A toxin receptor . These SNPs were used to investigate genetic linkage. Size differences of PCR products were discovered in CYP9A1, which was mapped to chromosome 7 by restriction fragment length polymorphism studies, and ryanodine receptor genes; however, these two genes were not linked with any other genes.; The sex linkage of TPI (triosephosphate isomerase ) and JHE (juvenile hormone esterase) was observed also in test cross families. JHE is important in the hydrolytic deactivation of the natural juvenile hormone and this is the first report of its sex linkage.; AceIn (acetylcholinesterase insensitivity), which was genetically linked to methyl parathion resistance and IDH-2 (isocitrate dehydrogenase-2) placing it on chromosome 2, was scored for genotype using an assay of enzyme inhibition. However, independent assortment of AceIn, y, yes, CYP6B10, CYP9A1, ryanodine receptor and hscp was observed in test crosses and formed the basis of a new genetic map composed of visible markers, SNPs and polymorphisms in the size of short segments of amplified genomic DNA.; Negative correlation of the susceptibility to chlorfenapyr with the susceptibility to cypermethrin was observed in the cypermethrin-resistant Dalzell98 strain and the pyrethroid-susceptible YYES strain. This observation confirmed previous reports of this phenomen... |
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