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. 2021 May 6;81(9):2031–2040.e8. doi: 10.1016/j.molcel.2021.03.020

Figure 1.

Figure 1

Pharmacological activation of non-canonical autophagy promotes ATG8-PS lipidation in cells

(A) Confocal images of WT and ATG13−/− MCF10A cells upon activation of canonical (PP242/BafA1) and non-canonical autophagy (monensin). Scale bar: 20 μm.

(B) Coomassie staining of GFP-IPs and western blotting of cells treated as in (A).

(C) C-terminal peptides of hLC3A conjugated to the PE or PS headgroup. Predicted molecular weights (MWs) are indicated.

(D) Collision-induced dissociation (CID) mass spectra of unmodified, PE-modified, or PS-modified hLC3A C-terminal peptides. Monoisotopic mass shifts: 197.05, glycerophosphoethanolamine (from PE); 241.04, glycerophosphoserine (from PS); arrowheads denote y8 ion peaks as examples.

(E–H) Normalized mass spectrometry analysis of hLC3A-PE and hLC3A-PS in WT (E and F) and ATG13−/− (G and H) cells.

(I–K) Analysis of endogenous GABARAPL2 in HeLa cells by western blotting and mass spectrometry.

Data represent means from three independent experiments. ∗p < 0.03 and ∗∗p < 0.002, paired t test. See also Figure S2.