Journal
AUTOPHAGY
Volume 10, Issue 4, Pages 708-709Publisher
LANDES BIOSCIENCE
DOI: 10.4161/auto.28103
Keywords
COPII; macroautophagy; TRAPPIII; Ypt1; Atg1
Categories
Funding
- Howard Hughes Medical Institute Funding Source: Medline
- NIGMS NIH HHS [GM0622580, R01 GM080616, GM080616] Funding Source: Medline
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A major unanswered question in the field of autophagy is how the double-membrane phagophore is formed. As this membrane expands, it engulfs proteins and organelles that are destined for degradation and then seals to form an autophagosome. A growing consensus in the field is that a subdomain of the ER initiates formation of the phagophore. We show that ER-derived COPII-coated vesicles, which bud from a specialized domain of the ER called the ER exit site (ERES), are a source of this membrane. This finding will now pave the way for a biochemical description of the early steps of phagophore initiation.
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