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Methionine but Not Folinic Acid or Vitamin B-12 Alters the Frequency of Neural Tube Defects in Axd Mutant Mice¹

Bureau of Biological Research, Nelson Laboratory, Rutgers University, Piscataway, NJ 08854

The Axd (axial defects) mutation, which causes open neural tube defects (NTD) in 25–30% of d 14 mouse embryos of heterozygous (Axd/+) matings and curly tails (CT) in 31%, can be useful in studying neurovertebral morphogenesis. Current interest focuses on the role of methionine in neurulation, because supplementation of dams with this essential amino acid (70 mg/kg body wt) has been shown to reduce by 41% the incidence of NTD among embryos of Axd/+ x Axd/+ crosses when administered on d 8 and 9 of pregnancy. The present experiments were undertaken to determine whether supplementation of dams with a higher dose of methionine could effect a greater level of remediation. At a dose of 180 mg/kg body wt, the amino acid produced a reduction in NTD of 47%, similar to that produced at 70 mg/kg body wt. Supplementation of dams of reciprocal matings of Axd/+ x BALB/cByJ or CF-1 mice allowed assessment of the effects of methionine in heterozygous embryos, which exhibit CT. The amino acid had no effect on Axd/+ embryos from the BALB crosses, but the frequency of CT declined significantly among embryos of the CF-1 outcrosses. Maternal supplements of folinic acid (33 mg/kg) or vitamin B-12 (330 mg/kg) did not alter the incidence of NTD or CT among Axd embryos. No difference in methionine concentration was detected in the serum of Axd/+ and +/+ dams.

KEY WORDS: • neural tube defects • folinic acid • methionine • vitamin B-12 • mice

¹ Supported by The Spina Bifida Association of America, The Spina Bifida Coalition of New Jersey, the Research Council of Rutgers University, the Charles and Johanna Busch Memorial Fund, and the Mary and Ernest Bowden Memorial Fund.

² To whom correspondence should be addressed.

Manuscript received 27 July 1992. Revision accepted 21 September 1992.

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