Abstract
Autophagy is important for the degradation of bulk cytoplasm, long-lived proteins, and entire organelles. In lower eukaryotes, autophagy functions as a cell death mechanism or as a stress response during development. However, autophagy's significance in vertebrate development, and the role (if any) of vertebrate-specific factors in its regulation, remains unexplained. Through careful analysis of the current autophagy gene mutant mouse models, we propose that in mammals, autophagy may be involved in specific cytosolic rearrangements needed for proliferation, death, and differentiation during embryogenesis and postnatal development. Thus, autophagy is a process of cytosolic "renovation," crucial in cell fate decisions.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Adaptor Proteins, Signal Transducing
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Animals
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Apoptosis Regulatory Proteins
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Autophagy / physiology*
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Autophagy-Related Protein 5
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Autophagy-Related Protein 7
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Autophagy-Related Proteins
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Beclin-1
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Cell Death / physiology*
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Cell Differentiation
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Cell Proliferation
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Cell Survival
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Disease Models, Animal
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Humans
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Mice
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Microtubule-Associated Proteins / genetics
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Microtubule-Associated Proteins / metabolism
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Morphogenesis*
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Phagosomes / metabolism
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Protein Kinases / genetics
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Protein Kinases / metabolism
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Proteins / genetics
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Proteins / metabolism
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Saccharomyces cerevisiae Proteins / genetics
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Saccharomyces cerevisiae Proteins / metabolism
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Signal Transduction / physiology
Substances
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Adaptor Proteins, Signal Transducing
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Ambra1 protein, mouse
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Apoptosis Regulatory Proteins
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Atg5 protein, mouse
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Atg7 protein, mouse
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Autophagy-Related Protein 5
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Autophagy-Related Proteins
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Beclin-1
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Becn1 protein, mouse
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Map1lc3b protein, mouse
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Microtubule-Associated Proteins
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Proteins
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Saccharomyces cerevisiae Proteins
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Protein Kinases
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ATG1 protein, S cerevisiae
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Autophagy-Related Protein 7