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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Effects of H-2 and vitamin A on eye defects in congenic mice.

Pregnant mice congenic with C57BL/10 (B10.A, B10.BR, B10.D2, B10.A(2R), B10.A(5R), B10.A(15R), B10.A(1R), B10.A(18R), and B10.OL) were fed Purina Mouse Chow or the same diet plus 200 IU of vitamin A daily. The pregnant dams were sacrificed on the 18th day of gestation and the fetuses were sexed and examined for defects in eye development. It was found that the frequency of microphthalmia and anophthalmia in the female progeny of mice fed Mouse Chow was 7.4-9.2% in B10.A and B10.BR, 4.0-5.5% in B10.A(18R), B10, B10.A(5R), B10.A(1R), B10.A(15R), and B10.A(2R), and 0.8% and 1.4% in B10.D2 and B10.OL mice, respectively. On average, the frequency of these defects in the female progeny was 6.2 times greater than that in males (P less than 0.001). The right eye was 5.8 times more often affected than the left (P less than 0.001). The addition of vitamin A to the diet increased the frequency of these eye abnormalities in all strains, suggesting that this effect is not mediated by loci associated with H-2, as is the case with vitamin A-enhanced cleft palate. The addition of vitamin A to the diet did not affect the ratios of affected males to females, affected right to left eye, or microphthalmia to anophthalmia. The results suggest that there are two loci on chromosome 17, one centromeric to E beta and one telemeric to C4, that interact to determine to some degree the frequency of microphthalmia and anophthalmia.[1]


  1. Effects of H-2 and vitamin A on eye defects in congenic mice. Tyan, M.L. Proc. Soc. Exp. Biol. Med. (1992) [Pubmed]
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