Journal
DEVELOPMENTAL CELL
Volume 39, Issue 1, Pages 116-130Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2016.09.001
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Funding
- JST PRESTO
- Funding Program for Next Generation World-Leading Researchers [LS043]
- JSPS KAKENHI [25111005]
- [25*7082]
- Grants-in-Aid for Scientific Research [16H06167, 25111005, 15H05637, 16H01194] Funding Source: KAKEN
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Autophagy is a cytoplasmic degradation system that is important for starvation adaptation and cellular quality control. Previously, we reported that Atg5-null mice are neonatal lethal; however, the exact cause of their death remains unknown. Here, we show that restoration of ATG5 in the brain is sufficient to rescue Atg5-null mice from neonatal lethality. This suggests that neuronal dysfunction, including suckling failure, is the primary cause of the death of Atg5-null neonates, which would further be accelerated by nutrient insufficiency due to a systemic failure in autophagy. The rescued Atg5-null mouse model, as a resource, allows us to investigate the physiological roles of autophagy in the whole body after the neonatal period. These rescued mice demonstrate previously unappreciated abnormalities such as hypogonadism and iron-deficiency anemia. These observations provide new insights into the physiological roles of the autophagy factor ATG5.
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