Anticoagulant rodenticides are commonly used to control rodent pests worldwide. They specifically inhibit the vitamin K epoxide reductase (VKORC1)， which is an enzyme encoded by the gene， involved in the recycling of vitamin K. Therefore， they prevent blood clotting. Numerous mutations of gene were reported in rodents， and some are involved in the resistant to rodenticides phenotype. Two hundred and sixty-six mice tails were received from 65 different locations in France. Coding sequences of gene were sequenced in order to detect mutations. Consequences of the observed mutations were evaluated by the use of recombinant VKORC1. More than 70% of mice presented mutations. Among these mice， 80% were h... More
Anticoagulant rodenticides are commonly used to control rodent pests worldwide. They specifically inhibit the vitamin K epoxide reductase (VKORC1)， which is an enzyme encoded by the gene， involved in the recycling of vitamin K. Therefore， they prevent blood clotting. Numerous mutations of gene were reported in rodents， and some are involved in the resistant to rodenticides phenotype. Two hundred and sixty-six mice tails were received from 65 different locations in France. Coding sequences of gene were sequenced in order to detect mutations. Consequences of the observed mutations were evaluated by the use of recombinant VKORC1. More than 70% of mice presented mutations. Among these mice， 80% were homozygous. Contrary to brown rats for which only one predominant genotype was found in France， nine missense single mutations and four double mutations were observed in house mice. The single mutations lead to resistance to first-generation antivitamin K (AVKs) only and are certainly associated with the use of these first-generation molecules by nonprofessionals for the control of mice populations. The double mutations， probably obtained by genetic recombination， lead to in vitro resistance to all AVKs. They must be regarded as an adaptive evolution to the current use of second-generation AVKs. The intensive use of first-generation anticoagulants probably allowed the selection of a high diversity of mutations， which makes possible the genetic recombination and consequently provokes the emergence of the more resistant mutated described to date.
