Linkage of acetylcholinesterase insensitivity to methyl parathion resistance in Heliothis virescens

• Published in: Biochemical genetics Vol. 34; no. 7/8; pp. 297 - 312
• Main Authors: Gilbert, R.D. (Clemson University, Clemson, SC.), Bryson, P.K, Brown, T.M
• Format: Journal Article
• Language: English
• Published: United States 01-08-1996
• Subjects: ACETILCOLINESTERASA; ACETYLCHOLINESTERASE; Acetylcholinesterase - drug effects; Acetylcholinesterase - genetics; Animals; Cholinesterase Inhibitors; Crosses, Genetic; Genes, Insect; Genetic Linkage; Genotype; HELIOTHIS; Heliothis virescens; Insecticide Resistance - genetics; Methyl Parathion; METIL PARATION; Moths; Nicotiana tabacum; PARATHION METHYL
• ISSN: 0006-2928; 1573-4927
• DOI: 10.1007/BF02399949

Resistance to methyl parathion insecticide has evolved in the tobacco budworm, Heliothis virescens, and several biochemical mechanisms have been identified in various strains. Reduced sensitivity of acetylcholinesterase to inhibition by methyl paraoxon, the active metabolite of the insecticide, is controlled by a single autosomal locus, AceIn. We report that AceIn is genetically linked to methyl parathion resistance, which is expressed as a dominant gene. Methyl parathion-resistant and -susceptible strains were intercrossed and the resulting mixed colony was heterozygous at AceIn. Pair matings from the mixed colony were chosen, on the basis of AceIn genotype only, to establish strains Ace-S and Ace-R, homozygous for AceIn(SS) and AceIn(RR), respectively. The Ace-R strain was 15.9-fold resistant compared to AceIn(SS), while hybrid progeny expressed 24.6-fold resistance, demonstrating dominant inheritance of resistance. When progeny of the backcross (Ace-S X Ace-R) to Ace-S were exposed to a discriminating dose of methyl parathion, 24.5% survived as predicted by the model of a single resistance gene. Survivors displayed only the AceIn(RS) genotype, demonstrating a linkage disequilibrium which was highly significant. Assuming that no other resistance genes are linked closely to AceIn, it would appear that AceIn is a powerful gene for resistance, conferring a resistance proportional to the slower rate of inhibition in the resistant enzyme. The contribution of AceIn to resistance relative to detoxicative genes and the possible interaction of resistance genes are discussed