Abstract: |
The genetic pathways that control development of the early mammalian embryo have remained poorly understood, in part because the systematic mutant screens that have been so successful in the identification of genes and pathways that direct embryonic development in Drosophila, Caenorhabditis elegans, and zebrafish have not been applied to mammalian embryogenesis. Here we demonstrate that chemical mutagenesis with ethylnitrosourea can be combined with the resources of mouse genomics to identify new genes that are essential for mammalian embryogenesis. A pilot screen for abnormal morphological phenotypes of midgestation embryos identified five mutant lines; the phenotypes of four of the lines are caused by recessive traits that map to single regions of the genome. Three mutant lines display defects in neural tube closure: one is caused by an allele of the open brain (opb) locus, one defines a previously unknown locus, and one has a complex genetic basis. Two mutations produce novel early phenotypes and map to regions of the genome not previously implicated in embryonic patterning. |
Keywords: |
mutation; nonhuman; mouse; phenotype; mammalia; animals; mice; embryo; embryo development; embryo pattern formation; morphogenesis; mice, inbred c57bl; gene mapping; caenorhabditis elegans; mice, inbred cba; genetic screening; ethylnitrosourea; lethal mutant; genetic markers; danio rerio; chromosome mapping; dna polymorphism; genes, lethal; neural tube defect; mice, inbred c3h; autosomal recessive inheritance; chemical mutagenesis; neural tube defects; exencephaly; genes, recessive; male; female; priority journal; article
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