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Title: NUTRITIONAL EPIGENETICS IN AXIN-FUSED (AXIN[FU])MICE: KINKY "TALES" ABOUT MOM'S DIET

Author
item Waterland, Robert
item SHI, XIN - BAYLOR COLL OF MEDICINE
item LIN, JUAN-RU - BAYLOR COLL OF MEDICINE
item SMITH, CHARLOTTE - BAYLOR COLL OF MEDICINE

Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: 1/26/2005
Publication Date: 4/2/2005
Citation: Waterland, R.A., Shi, X., Lin, J-R., Smith, C.A. 2005. Nutritional epigenetics in Axin-fused (Axin[Fu]) mice: Kinky "tales" about mom's diet [abstract]. The Federation of American Societies for Experimental Biology Conference. Part I(abstract 161.2):A218-A219.

Interpretive Summary: Not Required for an Abstract.

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.