Technical Abstract: The murine Axin[Fu] mutation shares many similarities with the viable yellow agouti (A[vy]) mutation, at which offspring epigenotype is influenced by maternal diet. We therefore wished to determine if dietary methyl donor supplementation during development increases Axin[Fu] CpG methylation and ameliorates the kinky-tail phenotype of Axin[Fu]/+ mice. C57 females were assigned to either NIH-31 diet or NIH-31 supplemented with extra folic acid, vitamin B[12], betaine, and choline two weeks before mating with Axin[Fu]/+ males. Offspring were classified for tail phenotype and DNA was isolated for genotyping and quantitation of Axin[Fu] site-specific CpG methylation. With only 5 litters per group studied thus far, maternal supplementation is reducing incidence of tail kinking among Axin[Fu]/+ offspring (41% vs. 56% affected, p<0.05). Surprisingly, though fewer supplemented offspring have tail kinks, those who do have more kinks than affected unsupplemented offspring (3.8 ± 0.5 vs. 1.9 ± 0.3, mean ± sem, p<0.001). Data on Axin[Fu]/+ offspring tail phenotype and Axin[Fu] CpG methylation shall be presented on a minimum of 10 litters per group. Our results, coupled with a bioinformatic comparison of the Axin[Fu] and A[vy] genomic regions, will yield insights into the genomic characteristics that render specific retrotransposon-associated genes epigenetically labile to the influence of early nutrition.