In Vivo Analysis of Autophagy in Response to Nutrient Starvation Using Transgenic Mice Expressing a Fluorescent Autophagosome Marker

2. Zero hunger 0301 basic medicine 570 0303 health sciences Saccharomyces cerevisiae Proteins Green Fluorescent Proteins 610 Mice, Transgenic Autophagy-Related Protein 8 Family Luminescent Proteins Mice 03 medical and health sciences Starvation Phagosomes Vacuoles Autophagy Tumor Cells, Cultured Animals Tissue Distribution Lysosomes Microscopy, Immunoelectron Microtubule-Associated Proteins
DOI: 10.1091/mbc.e03-09-0704 Publication Date: 2003-12-30T01:14:01Z
ABSTRACT
Macroautophagy mediates the bulk degradation of cytoplasmic components. It accounts for the degradation of most long-lived proteins: cytoplasmic constituents, including organelles, are sequestered into autophagosomes, which subsequently fuse with lysosomes, where degradation occurs. Although the possible involvement of autophagy in homeostasis, development, cell death, and pathogenesis has been repeatedly pointed out, systematic in vivo analysis has not been performed in mammals, mainly because of a limitation of monitoring methods. To understand where and when autophagy occurs in vivo, we have generated transgenic mice systemically expressing GFP fused to LC3, which is a mammalian homologue of yeast Atg8 (Aut7/Apg8) and serves as a marker protein for autophagosomes. Fluorescence microscopic analyses revealed that autophagy is differently induced by nutrient starvation in most tissues. In some tissues, autophagy even occurs actively without starvation treatments. Our results suggest that the regulation of autophagy is organ dependent and the role of autophagy is not restricted to the starvation response. This transgenic mouse model is a useful tool to study mammalian autophagy.
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