Skip to main content
. 2020 Feb 3;21(3):e48412. doi: 10.15252/embr.201948412

Figure 5. ATG2A‐LIR is essential for phagophore formation.

Figure 5

  • A–C
    U2OS ATG2A/B double‐knockout (DKO) cells or DKO reconstituted with ATG2A‐WT, ATG2A‐mLIR (FCIL/AAAA) or ATG2A‐mYFS (YFS/AAA) were starved for 2 h, fixed and stained for LC3B (green) or WIPI2 (magenta), (B) ATG9A (magenta) or (C) GABARAP (Magenta) and imaged using a Zeiss 880 AiryScan super‐resolution confocal microscope. Images are representatives of n = 3 independent experiments. Scale bar 10 μm.
  • D
    Transmission electron micrographs of ATG2A/B DKO cells (upper left), DKO + ATG2A‐WT (upper right), DKO+ ATG2A‐mLIR (lower left) and DKO+ATG2A‐mYFS (lower right) starved (EBSS) for 2 h. Clustered small vesicles (open arrowheads; DKO and DKO‐mLIR) and autophagosomes (closed arrow heads, DKO+ATG2A‐WT and DKO+ATG2A‐mYFS) indicated. Images are representative of n = 3 independent experiments. Scale bar 500 nm. ER = endoplasmic reticulum; N = nucleus; Mt = mitochondria; G = Golgi; AP = autophagosome.
  • E
    Model of ATG2 function based on the current knowledge. ATG2A localizes to ER membranes and facilitates lipid transfer from the ER to the growing phagophore. ATG2 interaction with GABARAP/GABARAP‐L1 is essential for anchoring ATG2 to growing phagophore and mutation of the GABARAP interaction region results in the formation of immature phagophores.