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TFEB controls retromer expression in response to nutrient availability.

Rachel Curnock1, Alessia Calcagni2, Andrea Ballabio2,3,4

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|November 8, 2019
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Summary
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Cells adapt to low nutrients by increasing surface transporters. Transcription factor EB (TFEB) upregulates retromer, a protein complex essential for recycling, to enhance nutrient uptake.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Endosomal recycling is crucial for maintaining cell surface nutrient transporters.
  • The integration of nutrient availability with recycling pathways remains poorly understood.

Purpose of the Study:

  • To investigate the mechanisms by which cells adapt nutrient transporter abundance to amino acid availability.
  • To elucidate the role of endosomal recycling machinery in adaptive nutrient uptake.

Main Methods:

  • Studied recycling of human glutamine transporters ASCT2 (SLC1A5), LAT1 (SLC7A5), SNAT1 (SLC38A1), and SNAT2 (SLC38A2).
  • Investigated the role of the retromer complex in SNAT2 trafficking.
  • Analyzed the transcriptional regulation of retromer genes (VPS35, VPS26A) by transcription factor EB (TFEB) and MiTF/TFE family members.

Main Results:

  • Amino acid restriction leads to adaptive cell surface delivery of SNAT2, dependent on the retromer complex.
  • Complete amino acid starvation or glutamine depletion upregulates retromer expression.
  • TFEB and MiTF/TFE family members directly regulate retromer gene promoters via CLEAR elements.

Conclusions:

  • Retromer-mediated endosomal recycling is essential for adaptive nutrient acquisition.
  • TFEB-driven upregulation of retromer expression facilitates nutrient uptake under starvation conditions.
  • This pathway represents a critical cellular adaptation to nutrient scarcity.