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Plasticity within the niche ensures the maintenance of a Sox2+ stem cell population in the mouse incisor.

Authors
  • Sanz-Navarro, Maria1, 2
  • Seidel, Kerstin3
  • Sun, Zhao4
  • Bertonnier-Brouty, Ludivine1, 5
  • Amendt, Brad A4, 6
  • Klein, Ophir D3, 7
  • Michon, Frederic8, 9
  • 1 Helsinki Institute of Life Sciences, Institute of Biotechnology, University of Helsinki, 00014 Helsinki, Finland. , (Finland)
  • 2 Orthodontics, Department of Oral and Maxillofacial Diseases, University of Helsinki, 00290 Helsinki, Finland. , (Finland)
  • 3 Department of Orofacial Sciences and Program in Craniofacial Biology, UCSF, San Francisco, CA 94143, USA.
  • 4 Department of Anatomy and Cell Biology, and the Craniofacial Anomalies Research Center, The University of Iowa, Iowa City, IA 52242, USA. , (Mali)
  • 5 Département de Biologie, École Normale Supérieure de Lyon, Université de Lyon, 69007 Lyon, France. , (France)
  • 6 College of Dentistry, The University of Iowa, Iowa City, IA 52242, USA.
  • 7 Department of Pediatrics and Institute for Human Genetics, University of California San Francisco, San Francisco, CA 94143, USA.
  • 8 Helsinki Institute of Life Sciences, Institute of Biotechnology, University of Helsinki, 00014 Helsinki, Finland [email protected] , (Finland)
  • 9 Keele Medical School and Institute for Science and Technology in Medicine, Keele University, Keele ST5 5BG, UK.
Type
Published Article
Journal
Development
Publisher
The Company of Biologists
Publication Date
Jan 08, 2018
Volume
145
Issue
1
Identifiers
DOI: 10.1242/dev.155929
PMID: 29180573
Source
Medline
Keywords
License
Unknown

Abstract

In mice, the incisors grow throughout the animal's life, and this continuous renewal is driven by dental epithelial and mesenchymal stem cells. Sox2 is a principal marker of the epithelial stem cells that reside in the mouse incisor stem cell niche, called the labial cervical loop, but relatively little is known about the role of the Sox2+ stem cell population. In this study, we show that conditional deletion of Sox2 in the embryonic incisor epithelium leads to growth defects and impairment of ameloblast lineage commitment. Deletion of Sox2 specifically in Sox2+ cells during incisor renewal revealed cellular plasticity that leads to the relatively rapid restoration of a Sox2-expressing cell population. Furthermore, we show that Lgr5-expressing cells are a subpopulation of dental Sox2+ cells that also arise from Sox2+ cells during tooth formation. Finally, we show that the embryonic and adult Sox2+ populations are regulated by distinct signalling pathways, which is reflected in their distinct transcriptomic signatures. Together, our findings demonstrate that a Sox2+ stem cell population can be regenerated from Sox2- cells, reinforcing its importance for incisor homeostasis.

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