Atg8 family LC3/GABARAP proteins are crucial for autophagosome–lysosome fusion but not autophagosome formation during PINK1/Parkin mitophagy and starvation

By T. Nguyen, B. Padman, Joanne L. Usher, V. Oorschot, G. Ramm, M. Lazarou. Journal of Cell Biology, 2016

595 citations recorded by the source corpus.

Current autophagy models suggest that Atg8 family LC3/GABARAP proteins are essential mediators of autophagosome biogenesis. Nguyen et al. exploit CRISPR/Cas9-generated knockouts of the LC3 or GABARAP subfamilies, or both subfamilies, to show that Atg8s are dispensable for autophagosome biogenesis but essential for autophagosome–lysosome fusion.

Subfields: Epidemiology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/0752e0ad952dc0abe5a74630749c19c6ceb9b7e6

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In Epidemiology

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Citations in the corpus

• Molecular mechanisms and physiological functions of mitophagy (2021, unknown): “GABARAP subfamily proteins localize on mature autophagosome and associate with PLEKHM1 at the lysosome to facilitate autophagosome – lysosome fusion during PINK1/Parkin-mediated mitophagy (Nguyen et al , 2016).”
• Selective Autophagy: ATG8 Family Proteins, LIR Motifs and Cargo Receptors. (2020, methodology): “Also, the kinetics of autophagosome maturation are severely affected making the entire process very inefficient without functional ATG8 proteins [35].”
• Monitoring and Measuring Autophagy (2017, background): “Recently, residual autophagic activity, although significantly lower than in wild-type cells, has been reported in autophagy conjugation system-deficient cells, where abnormal autophagosomes that have lost the autophagosome marker LC3 are still formed and degraded by lysosomes [24,40,55].”