Autophagy is an essential homeostatic process at the interface of membrane trafficking, quality control, the immune response, and metabolism. Fundamental analyses of the autophagic process are needed to guide investigations of the role and regulation of autophagy in aging and diseases such as neurodegeneration, cancer, infection and immunity, inflammation and allergy, and metabolic diseases. In this special collection, JCB Board member Hong Zhang and Senior Scientific Editor Melina Casadio revisit some of the most exciting articles recently published in JCB that advance our understanding of the mechanisms and disease relevance of autophagy. Papers were selected based on topic and number of reader requests for the full-text and PDF versions of the article. We hope you enjoy this special collection and look forward to your feedback on (https://twitter.com/JCellBiol)Twitter and (https://www.facebook.com/JCellBiol)Facebook.
Image © 2018 Zhao and Zhang: Overview of the autophagy pathway. Autophagosomes are generated at PI(3)P-enriched subdomains of the ER, called omegasomes (Ω). A cup-shaped autophagosomal precursor structure, the IM, forms in close association with the omegasome. Upon closure of the IM, cytoplasmic contents are enclosed in double-membrane autophagosomes, also known as AVi. Autophagosomes undergo a series of fusion processes with various endolysosomal compartments, including the earliest vesicular endocytic vesicles (EVE), early endosomes (EE), MVBs, and LEs/lysosomes to form amphisomes, also known as AVi/d. Amphisomes finally mature into functional autolysosomes, also called AVd.(p)
Lysosome, Metabolism, Infection, Immunity, ATG, SNARE, Autophagy, Membrane trafficking, Autophagosome, Mitophagy