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After the  vkorc1  gene was first identified, changes occurring in the gene have been considered one of the main reasons of reduced susceptibility of house mice to anticoagulants. A no-choice feeding test was conducted according to standard EPPO ( 2004 ) methodology. Animals were fed for 21 days on baits containing difenacoum 0.005%. All animals were bromadiolone-resistant. Seven months earlier, all test animals had survived a 21-day bromadiolone (0.005%) no-choice feeding test, and sequencing of their  vkorc1  gene had revealed the presence of Tyr139Cys and Leu1258Ser/Tyr139Cys VKOR variant. There were no survivors in the no-choice difenacoum feeding test. Consumption was not affected by VKOR variant, sex or genotype. A higher lethal dose was confirmed for Leu128Ser/Tyr139Cys than Tyr139Cys carriers, for females than males, and for homozygotes than heterozygotes. Our research showed that difenacoum 0.005% was effective against house mice carrying the Tyr139Cys VKOR variant, whether it occurred independently or in combination with the Leu128Ser variant in the  Vkorc1  gene.

Susceptibility of house mouse carriers of Tyr139Cys and Leu128Ser/Tyr139Cys VKOR variants to difenacoum