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S Schmidt Toxicology, Department of Human Molecular Genetics, Research Group Neurogenetics, Departments of

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A Hommel Toxicology, Department of Human Molecular Genetics, Research Group Neurogenetics, Departments of

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V Gawlik Toxicology, Department of Human Molecular Genetics, Research Group Neurogenetics, Departments of

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R Augustin Toxicology, Department of Human Molecular Genetics, Research Group Neurogenetics, Departments of

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N Junicke Toxicology, Department of Human Molecular Genetics, Research Group Neurogenetics, Departments of

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S Florian Toxicology, Department of Human Molecular Genetics, Research Group Neurogenetics, Departments of

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M Richter Toxicology, Department of Human Molecular Genetics, Research Group Neurogenetics, Departments of

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D J Walther Toxicology, Department of Human Molecular Genetics, Research Group Neurogenetics, Departments of

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A Schürmann Toxicology, Department of Human Molecular Genetics, Research Group Neurogenetics, Departments of

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Deletion of glucose transporter gene Slc2a3 (GLUT3) has previously been reported to result in embryonic lethality. Here, we define the exact time point of growth arrest and subsequent death of the embryo. Slc2a3 −/− morulae and blastocysts developed normally, implanted in vivo, and formed egg-cylinder-stage embryos that appeared normal until day 6.0. At day 6.5, apoptosis was detected in the ectodermal cells of Slc2a3 −/− embryos resulting in severe disorganization and growth retardation at day 7.5 and complete loss of embryos at day 12.5. GLUT3 was detected in placental cone, in the visceral ectoderm and in the mesoderm of 7.5-day-old wild-type embryos. Our data indicate that GLUT3 is essential for the development of early post-implanted embryos.

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