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TBC1D2B undergoes phase separation and mediates autophagy initiation.

Marina E Hoffmann1, Anne-Claire Jacomin1, Doris Popovic1

  • 1Molecular Signaling Group, Institute of Biochemistry II, Medical Faculty, Goethe University Frankfurt, Frankfurt, Germany.

Journal of Cellular Biochemistry
|January 16, 2024
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Summary

Small ubiquitin-like modifiers regulate autophagy. TBC1D2B protein binds to key autophagy complexes, is degraded by autophagy, and its liquid droplet formation suggests a role in phase separation for autophagy induction.

Keywords:
ATG8‐related proteinsGTPase‐activating proteinKIAA1055autophagyautophagy conjugation complexliquid–liquid phase separationphagophore formation

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Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Small ubiquitin-like modifiers (SUMs) from the ATG8 family are crucial regulators of autophagy.
  • Interaction with LC3-interacting region (LIR) proteins is vital for cargo sequestration and autophagosome-lysosome fusion.
  • RabGAP proteins of the TBC family have been shown to bind LC3/GABARAP proteins.

Purpose of the Study:

  • To investigate the function of TBC1D2B in autophagy.
  • To determine the role of TBC1D2B in the early stages of autophagy.
  • To explore the mechanism of TBC1D2B-dependent autophagy induction.

Main Methods:

  • Analysis of TBC1D2B's LIR motif.
  • Investigation of TBC1D2B binding to LC3/GABARAP and ATG12 complexes.
  • Observation of TBC1D2B degradation via autophagy.
  • Microscopy to study TBC1D2B condensation into liquid droplets upon autophagy induction.

Main Results:

  • TBC1D2B possesses a functional canonical LIR motif.
  • TBC1D2B interacts with both LC3/GABARAP and ATG12 conjugation complexes during early autophagy.
  • TBC1D2B undergoes autophagy-mediated degradation.
  • TBC1D2B forms liquid droplets upon autophagy induction, indicating a role in phase separation.

Conclusions:

  • TBC1D2B functions at an early stage of autophagy.
  • Phase separation is a potential mechanism underlying TBC1D2B-mediated autophagy induction.