TOR at the core of impaired regeneration

2018 ◽  
Vol 10 (422) ◽  
pp. eaar7508
Author(s):  
Christopher Hine
Keyword(s):  
Stem Cell ◽  
Tissue Regeneration ◽  
Target Of Rapamycin ◽  
Tor Signaling ◽  
Stem Cell Maintenance ◽  
The Core ◽  
Cell Maintenance

Repeated activation of target of rapamycin (TOR) signaling during tissue regeneration results in impaired stem cell maintenance and promotes aging.

scholarly journals Yap1-driven intestinal repair is controlled by group 3 innate lymphoid cells

2019 ◽  
Author(s):  
Mónica Romera-Hernández ◽  
Patricia Aparicio-Domingo ◽  
Natalie Papazian ◽  
Julien J. Karrich ◽  
Ferry Cornelissen ◽  
...  
Keyword(s):  
Stem Cell ◽  
Tissue Regeneration ◽  
Tissue Repair ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Stem Cell Maintenance ◽  
Epithelial Regeneration ◽  
Group 3 ◽  
Intestinal Repair ◽  
Cell Maintenance

SUMMARYTissue repair requires temporal control of progenitor cell proliferation and differentiation to replenish damaged cells. In response to acute insult, group 3 innate lymphoid cells (ILC3) regulate intestinal stem cell maintenance and subsequent tissue repair. ILC3-derived IL-22 is important for stem cell protection, but the mechanisms of ILC3-driven tissue regeneration remain incompletely defined. Here we report that group 3 innate lymphoid cell (ILC3)-driven epithelial proliferation and tissue regeneration are independent of IL-22. In contrast, ILC3 amplify the magnitude of Hippo-Yap1 signaling in intestinal crypt cells, ensuring adequate initiation of tissue repair and preventing excessive pathology. Mechanistically, ILC3-driven tissue repair is Stat3-independent, but involves activation of Src family kinases. Our findings reveal that ILC3-driven intestinal repair entails distinct transcriptional networks to control stem cell maintenance and epithelial regeneration which implies that tissue repair and crypt proliferation can be influenced by targeting innate immune cells independent of the well-established effects of IL-22.

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