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. Author manuscript; available in PMC: 2023 Mar 16.
Published in final edited form as: Sci Signal. 2023 Jan 31;16(770):eabo4457. doi: 10.1126/scisignal.abo4457

Fig. 1. Formation of autophagosomes at baseline and in response to stress in Becn1−/− deficient MEFs.

Fig. 1.

A) Representative immunofluorescent images and quantification of the total percentage of cells with GFP-LC3 positive vesicles in WT and Becn1−/− MEFs before (0h) or after (3h) bafilomycin A1 (Baf A1) treatment (100nm) (n=100 cells/group from 3 experiments). B) Representative Western blots for LC3 and p62 in WT and Becn1−/− MEFs at baseline (0h) and after (3h) bafilomycin A1 (Baf A1) treatment (100 nM). C) Quantification of LC3 and p62 protein levels. Actin was used as a loading control (n=4-5 independent experiments). D) Representative immunofluorescent images and quantification of the total percentage of cells with GFP-LC3 positive vesicles in WT and Becn1−/− MEFs before (0h) or after (3h) starvation (Starv) (n=100 cells/group from 3 experiments). E) Representative Western blot for LC3 in WT and Becn1−/− MEFs after starvation. F) Quantification of LC3I and LC3II protein levels (n=5 independent experiments). G) Representative immunofluorescent images and quantification of the total percentage of cells with GFP-LC3 positive vesicles in WT and Becn1−/− MEFs before (0h) or after (3h) FCCP treatment (10 μM) (n=100 cells/group from 3 experiments). H) Representative Western blot for LC3 in WT and Becn1−/− MEFs after 10 μM FCCP treatment. I) Quantification of LC3I and LC3II protein levels (n=4 independent experiments). Data are presented as means ± SEM. *p<0.05, **p<0.01, ***p<0.001, and ns = not significant by two-way analysis of variance (ANOVA) followed by Tukey’s multiple comparison test. Scale bars = 10 μm.