Premium
Autophagy‐related gene Atg5 is essential for astrocyte differentiation in the developing mouse cortex
Author(s) -
Wang Shukun,
Li Baoguo,
Qiao Huimin,
Lv Xiaohui,
Liang Qingli,
Shi Zixiao,
Xia Wenlong,
Ji Fen,
Jiao Jianwei
Publication year - 2014
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201338343
Subject(s) - autophagy , astrocyte , atg5 , biology , microbiology and biotechnology , gene , cortex (anatomy) , neuroscience , genetics , central nervous system , apoptosis
Astrocyte differentiation is essential for late embryonic brain development, and autophagy is active during this process. However, it is unknown whether and how autophagy regulates astrocyte differentiation. Here, we show that Atg5, which is necessary for autophagosome formation, regulates astrocyte differentiation. Atg5 deficiency represses the generation of astrocytes in vitro and in vivo . Conversely, Atg5 overexpression increases the number of astrocytes substantially. We show that Atg5 activates the JAK 2‐ STAT 3 pathway by degrading the inhibitory protein SOCS 2. The astrocyte differentiation defect caused by Atg5 loss can be rescued by human Atg5 overexpression, STAT 3 overexpression, and SOCS 2 knockdown. Together, these data demonstrate that Atg5 regulates astrocyte differentiation, with potential implications for brain disorders with autophagy deficiency.