4.8 Article

Thy1 marks a distinct population of slow-cycling stem cells in the mouse epidermis

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NATURE COMMUNICATIONS
卷 13, 期 1, 页码 -

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NATURE PORTFOLIO
DOI: 10.1038/s41467-022-31629-1

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  1. NIH [RO1GM60124]
  2. ISF [2751/20, 2124/19IPMP 1019045-2029637]
  3. EMBO Young Investigator program

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Koren and Feldman et al. discovered a distinct population of Thy1-expressing stem cells in the basal layer of the mouse epidermis that contribute to epidermal replenishment and wound repair. These stem cells display unique transcriptional signatures and exhibit slower cell cycle kinetics compared to basal epidermal progenitors. The ablation of Thy1(+) cells impairs epidermal homeostasis and repair, highlighting the critical role of these stem cells in maintaining the integrity of the epidermis.
Koren and Feldman et al. report a distinct population of Thy1-expressing stem cells in the basal layer of the mouse epidermis. These stem cells do not compete neutrally and contribute long-term to both epidermal replenishment and wound repair. The presence of distinct stem cells that maintain the interfollicular epidermis is highly debated. Here, we report a population of keratinocytes, marked by Thy1, in the basal layer of the interfollicular epidermis. We find that epidermal cells expressing differential levels of Thy1 display distinct transcriptional signatures. Thy1(+) keratinocytes do not express T cell markers, express a unique transcriptional profile, cycle significantly slower than basal epidermal progenitors and display significant expansion potential in vitro. Multicolor lineage tracing analyses and mathematical modeling reveal that Thy1(+) basal keratinocytes do not compete neutrally alike interfollicular progenitors and contribute long-term to both epidermal replenishment and wound repair. Importantly, ablation of Thy1(+) cells strongly impairs these processes, thus indicating the non-redundant function of Thy1(+) stem cells in the epidermis. Collectively, these results reveal a distinct stem cell population that plays a critical role in epidermal homeostasis and repair.

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