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S Schmidt, Pharmacology, German Institute of Human Nutrition, Potsdam-Rehbruecke, Germany
A Hommel, Pharmacology, German Institute of Human Nutrition, Potsdam-Rehbruecke, Germany
V Gawlik, Pharmacology, German Institute of Human Nutrition, Potsdam-Rehbruecke, Germany
R Augustin, Pharmacology, German Institute of Human Nutrition, Potsdam-Rehbruecke, Germany
N Junicke, Pharmacology, German Institute of Human Nutrition, Potsdam-Rehbrücke, Germany
S Florian, Toxicology, German Institute of Human Nutrition, Potsdam-Rehbrüke, Germany
M Richter, Pharmacology, German Institute of Human Nutrition, Potsdam-Rehbruecke, Germany
D Walther, Human Molecular Genetics, Max Planck Institute for Molecular Genetics, Berlin, Germany
D Montag, Research Group Neurogenetics, Leibniz-Institute for Molecular Genetics, Magdeburg, Germany
H Joost, Pharmacology, German Institute of Human Nutrition, Potsdam-Rehbruecke, Germany
A Schuermann, Pharmacology, German Institute of Human Nutrition, Potsdam-Rehbruecke, Germany

Correspondence: Annette Schuermann, Email: schuermann{at}dife.de

Abstract

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 blastocyts 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 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 ecdoderm and in the mesoderm of 7.5 days old wild type embryos. Our data indicate that GLUT3 is essential for the development of early post-implanted embryos.

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