Abstract

Dominant warfarin resistance and a recessive haemorrhagic trait are apparently controlled by the same allele Rw2. Twenty-eight F2 litters and 18 backcross litters of wild rats were scored for resistance when 8 weeks of age. There was a deficiency of resistant males in the F2 litters whereas phenotypic ratios were close to expectation in F2 females and backcrosses. Any deficiency of resistant males in F2 litters could be due to the selective death of the Rw2Rw2 genotype. The size of F2 and backcross litters at birth is similar whereas by 8 weeks the former are significantly smaller than the latter. Samples of rats from populations in mid Wales were scored for resistance. There was a significant decline in the frequency of phenotypic resistance in one large population (N≈500) starting when the frequency of the Rw2 allele was relatively low (c. 0·10–0·23). Since few alleles can be lost by selective death of Rw2Rw2 males in these circumstances it appears that, in the absence of warfarin, the heterozygote may also be at a selective disadvantage. Where rats are intensively poisoned with warfarin both Rw2 and its alternative Rw1 are maintained in populations by heterozygous advantage. The ecological unreality of the concept of segregational load is discussed. Strong selection influences the frequency of the alleles of Rw. Chance must also have an important role. Populations of rats in rural areas are widely scattered and sometimes small in size. There is an unpredictable amount of movement between these populations which occur in very heterogeneous environments.

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