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Submitted on September 22, 2003
Accepted on November 21, 2003
1 Washington University School of Medicine, Department of Obstetrics and Gynecology, 4911 Barnes Hospital Plaza, St. Louis, MO 63110
* To whom correspondence should be addressed. E-mail: moleyk{at}msnotes.wustl.edu.
During preimplantation development in the mouse, it is crucial that glucose metabolism not be compromised. Any decrease in glucose uptake at this stage in development can compromise the developing embryo. We have cloned another member of the glucose transporter family, GLUT9, which is expressed embryonically. Three different isoforms were identified. We have shown that two of the mouse GLUT9 isoforms transport glucose at a rate significantly greater than controls. Expression analysis of the preimplantation blastocyst identifies only the presence of the shorter GLUT9 isoform, RT-PCR and western immunoblot confirmed this finding. A differential pattern of expression was seen with GLUT9 present at the plasma membrane in 1- and 2-cell zygotes, and in an intracellular compartment in trophectoderm cells at a blastocyst stage. While blocking GLUT9 expression during preimplantation development had no effect on glucose transport or apoptosis, transfer of these embryos into pseudopregnant mice resulted in increased pregnancy loss, suggesting that GLUT9 is critical for early preimplantation development.
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