Journal
NATURE CELL BIOLOGY
Volume 12, Issue 6, Pages 572-U121Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncb2059
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Funding
- FNRS
- Human Frontier Science Program Organization (HFSPO)
- Schlumberger Foundation
- Wallonia Region
- Fondation Contre le Cancer
- Gaston Ithier
- European Research Council (ERC)
- EMBO Young Investigator Program
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Adult stem cells (SCs) are at high risk of accumulating deleterious mutations because they reside and self-renew in adult tissues for extended periods. Little is known about how adult SCs sense and respond to DNA damage within their natural niche. Here, using mouse epidermis as a model, we define the functional consequences and the molecular mechanisms by which adult SCs respond to DNA damage. We show that multipotent hair-follicle-bulge SCs have two important mechanisms for increasing their resistance to DNA-damage-induced cell death: higher expression of the anti-apoptotic gene Bcl-2 and transient stabilization of p53 after DNA damage in bulge SCs. The attenuated p53 activation is the consequence of a faster DNA repair activity, mediated by a higher non-homologous end joining (NHEJ) activity, induced by the key protein DNA-PK. Because NHEJ is an error-prone mechanism, this novel characteristic of adult SCs may have important implications in cancer development and ageing.
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