期刊
SCIENCE
卷 332, 期 6036, 页码 1429-1433出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1204592
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资金
- Italian Telethon Foundation
- Beyond Batten Disease Foundation
- European Research Council [250154]
- European Molecular Biology Organization
- Wellcome Trust
- U.K. Medical Research Council
- Intellectual and Developmental Disabilities Research Center at the Baylor College of Medicine [5 P30 HD024064]
- Medical Research Council [G0600194] Funding Source: researchfish
- MRC [G0600194] Funding Source: UKRI
- European Research Council (ERC) [250154] Funding Source: European Research Council (ERC)
Autophagy is a cellular catabolic process that relies on the cooperation of autophagosomes and lysosomes. During starvation, the cell expands both compartments to enhance degradation processes. We found that starvation activates a transcriptional program that controls major steps of the autophagic pathway, including autophagosome formation, autophagosome-lysosome fusion, and substrate degradation. The transcription factor EB (TFEB), a master gene for lysosomal biogenesis, coordinated this program by driving expression of autophagy and lysosomal genes. Nuclear localization and activity of TFEB were regulated by serine phosphorylation mediated by the extracellular signal-regulated kinase 2, whose activity was tuned by the levels of extracellular nutrients. Thus, a mitogen-activated protein kinase-dependent mechanism regulates autophagy by controlling the biogenesis and partnership of two distinct cellular organelles.
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