| First Author | Suh HN | Year | 2017 |
| Journal | Cell Rep | Volume | 21 |
| Issue | 9 | Pages | 2571-2584 |
| PubMed ID | 29186692 | Mgi Jnum | J:255239 |
| Mgi Id | MGI:6104108 | Doi | 10.1016/j.celrep.2017.10.118 |
| Citation | Suh HN, et al. (2017) Quiescence Exit of Tert(+) Stem Cells by Wnt/beta-Catenin Is Indispensable for Intestinal Regeneration. Cell Rep 21(9):2571-2584 |
| abstractText | Fine control of stem cell maintenance and activation is crucial for tissue homeostasis and regeneration. However, the mechanism of quiescence exit of Tert(+) intestinal stem cells (ISCs) remains unknown. Employing a Tert knockin (Tert(TCE/+)) mouse model, we found that Tert(+) cells are long-term label-retaining self-renewing cells, which are partially distinguished from the previously identified +4 ISCs. Tert(+) cells become mitotic upon irradiation (IR) injury. Conditional ablation of Tert(+) cells impairs IR-induced intestinal regeneration but not intestinal homeostasis. Upon IR injury, Wnt signaling is specifically activated in Tert(+) cells via the ROS-HIFs-transactivated Wnt2b signaling axis. Importantly, conditional knockout of beta-catenin/Ctnnb1 in Tert(+) cells undermines IR-induced quiescence exit of Tert(+) cells, which subsequently impedes intestinal regeneration. Our results that Wnt-signaling-induced activation of Tert(+) ISCs is indispensable for intestinal regeneration unveil the underlying mechanism for how Tert(+) stem cells undergo quiescence exit upon tissue injury. |
