Biochemical genetics of resistance to organophosphorus acaricides in three strains of the cattle tick, Boophilus microplus.
Three aspects of the biochemical genetics of resistance to organophosphorus compounds in the Biarra (B), Mackay (M) and Ridgelands (R) strains of the cattle tick B. microplus were studied. These were: decreased acetylcholinesterase (AChE) activity in adult brains of strains B and M; decreased AChE sensitivity to inhibitors in adult brains and in larvae of strains B, M and R; and increased detoxication in larvae and adult females of strain M. Comparisons were made with a susceptible reference strain (S). Microspectrophotometric estimations of AChE activity in histochemical preparations of whole brains showed that hybrids had levels of activity approximately intermediate between those of the parental strains. Homogenates of brains from hybrids assayed biochemically gave similar but more precise results which indicated that decreased brain AChE activity was neither recessive nor dominant (degree of dominance, D = +0-02) in strain B and incompletely recessive (D = -0-26) in strain M. The proportions of brains showing decreased AChE activity in testcross and F2 progenies indicated that decreased AChE activity in strains B and M is controlled by single autosomal genes. Inhibition of AChE at diagnostic concentrations of coroxon in brains of B, B x S hybrid and S types suggested that decreased sensitivity of AChE in strain B is incompletely dominant (D = +0-10). Kinetic studies on coroxon inhibition of AChE in brain homogenates of B, B x S hybrid and S types revealed the presence of each parental AChE component in hybrids in equal amounts and the absence of a hybrid enzyme. Dimethoxon inhibition of AChE in brains, their homogenates and larval homogenates of B, M and R types showed that decreased AChE sensitivity was a major mechanism of resistance to dimethoate strongly expressed in B x S and M x S hybrids. The proportion of brains showing decreased AChE sensitivity to coroxon in testocross and F2 progenies indicated that decreased AChE sensitivity in strain B is controlled by a single autosomal gene. The degree of dominance of increased degradative metabolism of coumaphos in strain M was variable; the hydrolytic rate in all M x S hybrids was similar to that of M but the overall detoxication rate in hybrids was lower. Genetic control of detoxication is discussed.
D000110:Acetylcholinesterase / Q000032:analysis*; D000818:Animals; D001921:Brain / Q000201:enzymology; D003372:Coumaphos / Q000031:analogs & derivatives / Q000378:metabolism; D003433:Crosses, Genetic; D004117:Dimethoate / Q000031:analogs & derivatives; D004351:Drug Resistance; D005260:Female; D005796:Genes; D005799:Genes, Dominant; D005808:Genes, Recessive; D008040:Genetic Linkage; D008297:Male; D009943:Organophosphorus Compounds; D012730:Sex Chromosomes; D013987:Ticks / Q000201:enzymology* / Q000378:metabolism
D009943:Organophosphorus Compounds; D000110:Acetylcholinesterase; D003372:Coumaphos; D004117:Dimethoate