Shanta Nag

TL;DR: Evidence is provided for the involvement of exocytic Q/t-SNAREs in autophagosome formation, acting in the recruitment of key autophagy components to the site of autophagic formation, and in regulating the organization of Atg9 into tubulovesicular clusters.

TL;DR: It is demonstrated that the E2-like enzyme, Atg3, facilitates LC3/GABARAP lipidation only on membranes exhibiting local lipid-packing defects, suggesting a physiologic role for this stress detection.

TL;DR: Lystad et al. identify distinct membrane binding regions in ATG16L1 and show that the β-isoform-specific C-terminal region is required for VPS34/ULK1/2-independent non-canonical autophagy.

TL;DR: A model whereby ATG 4B drives very fast priming of mammalian Atg8 proteins, whereas delipidation is inherently slow and regulated by all ATG4 homologs is suggested.

TL;DR: It is suggested that to support efficient production and consumption of autophagosomes, additional factors are essential including possibly ATG4B itself or one of its proteolytic products in the LC3 family.