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Glucose metabolism distinguishes TE from ICM fate during mammalian embryogenesis

Fangtao Chi, Mark S. Sharpley, Raghavendra Nagaraj, Shubhendu Sen Roy, Utpal Banerjee
doi: https://doi.org/10.1101/826875
Fangtao Chi
1Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA
2Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA
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Mark S. Sharpley
1Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA
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  • For correspondence: marksharpley@ucla.edu banerjee@mbi.ucla.edu
Raghavendra Nagaraj
1Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA
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Shubhendu Sen Roy
1Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA
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Utpal Banerjee
1Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA
2Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA
3Department of Biological Chemistry, University of California, Los Angeles, Los Angeles, CA 90095, USA
4Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, Los Angeles, CA 90095, USA
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  • For correspondence: marksharpley@ucla.edu banerjee@mbi.ucla.edu
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Summary

The mouse embryo undergoes compaction at the 8-cell stage and its transition to 16 cells generates polarity such that the outer apical cells are trophectoderm (TE) precursors and the inner cell mass (ICM) gives rise to the embryo. We report here, that this first cell fate specification event is controlled by glucose metabolism. Glucose does not fuel mitochondrial ATP (energy) generation and glycolysis is dispensable for blastocyst formation. Glucose does not help synthesize amino acids, fatty acids, and nucleobases. Instead, glucose metabolized by the hexosamine biosynthetic pathway (HBP) allows nuclear localization of YAP1, and the pentose phosphate pathway (PPP), along with sphingolipid (S1P) signaling, activates mTOR and allows translation of AP-2γ. YAP1, TEAD4 and AP-2γ physically interact to form a nuclear complex that controls TE-specific gene transcription. Glucose signaling has no role in ICM specification, but this cascade of events constituting “Developmental Metabolism” specifically controls the fate of TE cells.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted October 31, 2019.
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Glucose metabolism distinguishes TE from ICM fate during mammalian embryogenesis
Fangtao Chi, Mark S. Sharpley, Raghavendra Nagaraj, Shubhendu Sen Roy, Utpal Banerjee
bioRxiv 826875; doi: https://doi.org/10.1101/826875
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Glucose metabolism distinguishes TE from ICM fate during mammalian embryogenesis
Fangtao Chi, Mark S. Sharpley, Raghavendra Nagaraj, Shubhendu Sen Roy, Utpal Banerjee
bioRxiv 826875; doi: https://doi.org/10.1101/826875

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