| First Author | Yoshii SR | Year | 2016 |
| Journal | Dev Cell | Volume | 39 |
| Issue | 1 | Pages | 116-130 |
| PubMed ID | 27693508 | Mgi Jnum | J:236380 |
| Mgi Id | MGI:5805991 | Doi | 10.1016/j.devcel.2016.09.001 |
| Citation | Yoshii SR, et al. (2016) Systemic Analysis of Atg5-Null Mice Rescued from Neonatal Lethality by Transgenic ATG5 Expression in Neurons. Dev Cell 39(1):116-130 |
| abstractText | 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. |
