Inhibitor Report for: Formothion

Resistance to the organophosphorus acaricides diazinon, dimethoate and formothion in the Biarra (B), Mackay (M) and Ridgelands (R) strains respectively of the cattle tick B. microplus has been shown previously to be controlled in each strain by a single incompletely dominant autosomal genetic factor. A very similar mode of inheritance of fenthion resistance in strain B has now been demonstrated with no departure in degree of dominance of resistance from the mean value of +0-57 common to these strains exposed to these chemicals. No F1 larval progeny from the following crossings were appreciably more resistant than their parents to these chemicals: R x B--bromophos ethyl and fenthion; B x M--carbaryl, chlorfenvinphos, chlorpyrifos, diazinon, dimethoate, ethion, fenthion and formothion; M x R--chlorfenvinphos, diazinon, dimethoate, ethion, formothion. The field importance of this absence of overdominance is discussed. There were no susceptible double recessive F2 larval progeny of B x M crossings of F2 or F3 larval progeny of R x M crossings when tested against dimethoate to which the three parental types were similarly resistant; 1/16 of the larval progeny would be expected to be completely susceptible if the resistance genes were unlinked. F1 adult progeny of B x M and R x M crossings exhibited the incompletely recessive mutant-type decreased brain acetylcholinesterase (AChE) activity common to strains B, M and R, thus satisfying the test for allelism. No ticks with normal levels of brain AChE were detected in F2 adult progeny of B x M or R x M crossings. This evidence was strongly suggestive of a series of closely linked genes or alleles controlling dimethoate resistance and a series of alleles controlling decreased brain AChE activity in strains B, M and R.

Resistance to the organophosphorus acaricides diazinon, dimethoate and formothion in the Biarra (B), Mackay (M) and Ridgelands (R) strains respectively of the cattle tick B. microplus has been shown previously to be controlled in each strain by a single incompletely dominant autosomal genetic factor. A very similar mode of inheritance of fenthion resistance in strain B has now been demonstrated with no departure in degree of dominance of resistance from the mean value of +0-57 common to these strains exposed to these chemicals. No F1 larval progeny from the following crossings were appreciably more resistant than their parents to these chemicals: R x B--bromophos ethyl and fenthion; B x M--carbaryl, chlorfenvinphos, chlorpyrifos, diazinon, dimethoate, ethion, fenthion and formothion; M x R--chlorfenvinphos, diazinon, dimethoate, ethion, formothion. The field importance of this absence of overdominance is discussed. There were no susceptible double recessive F2 larval progeny of B x M crossings of F2 or F3 larval progeny of R x M crossings when tested against dimethoate to which the three parental types were similarly resistant; 1/16 of the larval progeny would be expected to be completely susceptible if the resistance genes were unlinked. F1 adult progeny of B x M and R x M crossings exhibited the incompletely recessive mutant-type decreased brain acetylcholinesterase (AChE) activity common to strains B, M and R, thus satisfying the test for allelism. No ticks with normal levels of brain AChE were detected in F2 adult progeny of B x M or R x M crossings. This evidence was strongly suggestive of a series of closely linked genes or alleles controlling dimethoate resistance and a series of alleles controlling decreased brain AChE activity in strains B, M and R.