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The primary defect in most mouse NTDs is failure of neural fold elevation. Most null mutations (&gt;90%) produce syndromes of multiple affected structures with high penetrance in homozygotes, whereas the \u201cmultifactorial\u201d strains and several null\u2010mutant heterozygotes and mutants with partial gene function (hypomorphs) have low\u2010penetrance nonsyndromic NTDs, like the majority of human NTDs. The normal functions of the mutated genes are diverse, with clusters in pathways of actin function, apoptosis, and chromatin methylation and structure. The female excess observed in human anencephaly is found in all mouse exencephaly mutants for which gender has been studied. Maternal agents, including folate, methionine, inositol, or alternative commercial diets, have specific preventative effects in eight mutants and strains. <jats:bold>CONCLUSIONS<\/jats:bold>: If the human homologs of the mouse NTD mutants contribute to risk of common human NTDs, it seems likely to be in multifactorial combinations of hypomorphs and low\u2010penetrance heterozygotes, as exemplified by mouse digenic mutants and the oligogenic SELH\/Bc strain. Birth Defects Research (Part A), 2007. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/bdra.20333","type":"journal-article","created":{"date-parts":[[2006,12,19]],"date-time":"2006-12-19T22:57:08Z","timestamp":1166569028000},"page":"187-210","source":"Crossref","is-referenced-by-count":279,"title":["Mouse mutants with neural tube closure defects and their role in understanding human neural tube defects"],"prefix":"10.1002","volume":"79","author":[{"given":"Muriel J.","family":"Harris","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Diana 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