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Excess methionine suppresses the methylation cycle and inhibits neural tube closure in mouse embryos
Author(s) -
Dunlevy Louisa P.E.,
Burren Katie A.,
Chitty Lyn S.,
Copp Andrew J.,
Greene Nicholas D.E.
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.04.020
Subject(s) - mesenchyme , neural tube , methionine , methylation , embryo , dna methylation , exencephaly , biology , microbiology and biotechnology , neural tube defect , andrology , chemistry , endocrinology , medicine , fetus , biochemistry , genetics , gene , gene expression , teratology , amino acid , pregnancy
Suppression of one‐carbon metabolism or insufficient methionine intake are suggested to increase risk of neural tube defects (NTD). Here, exogenous methionine unexpectedly caused frequent NTD in cultured mouse embryos. NTD were associated with reduced cranial mesenchyme cell density, which may result from a preceding reduction in proliferation. The abundance ratio of S ‐adenosylmethionine to S ‐adenosylhomocysteine was also decreased in treated embryos, suggesting methylation reactions may be suppressed. Such an effect is potentially causative as NTD were also observed when DNA methylation was specifically inhibited. Thus, reduced cranial mesenchyme density and impairment of critical methylation reactions may contribute to development of methionine‐induced NTD.