ISSN:
1573-4927
Keywords:
acetylcholinesterase gene
;
tobacco budworm
;
linkage analysis
;
insecticide resistance
;
microtiter plate analysis
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Chemistry and Pharmacology
Notes:
Abstract 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 thatAceIn is genetically linked to methyl parathion resistance, which is expressed as a dominant gene. Methyl parathionresistant and -susceptible strains were intercrossed and the resulting mixed colony was heterozygous atAceIn. Pair matings from the mixed colony were chosen, on the basis ofAceIn genotype only, to establish strains Ace-S and Ace-R, homozygous forAceIn SS andAceIn RR, respectively. The Ace-R strain was 15.9-fold resistant compared toAceIn SS, while hybrid progeny expressed 24.6-fold resistance, demonstrating dominant inheritance of resistance. When progeny of the backcross (Ace-S×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 theAceIn RS genotype, demonstrating a linkage disequilibrium which was highly significant. Assuming that no other resistance genes are linked closely toAceIn, it would appear thatAceIn is a powerful gene for resistance, conferring a resistance proportional to the slower rate of inhibition in the resistant enzyme. The contribution ofAceIn to resistance relative to detoxicative genes and the possible interaction of resistance genes are discussed.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF02399949
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