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Sox2 contributes to tooth development via Wnt signaling.

Authors
 Min-Jung Lee  ;  Eun-Jung Kim  ;  Keishi Otsu  ;  Hidemitsu Harada  ;  Han-Sung Jung 
Citation
 CELL AND TISSUE RESEARCH, Vol.365(1) : 77-84, 2016 
Journal Title
CELL AND TISSUE RESEARCH
ISSN
 0302-766X 
Issue Date
2016
MeSH
Animals ; Cell Movement ; Gene Expression Regulation, Developmental ; Gene Knockdown Techniques ; Mice ; RNA, Small Interfering/metabolism ; SOXB1 Transcription Factors/metabolism* ; Time Factors ; Tooth/embryology* ; Tooth/metabolism* ; Wnt Signaling Pathway*
Keywords
Cell migration ; DiI system ; Sox2 ; Tooth ; Wnt signaling
Abstract
The transcription factor Sox2 is a stem cell marker that dictates cell lineage. It has been shown to mark the epithelial stem cells of the continuously growing mouse incisors. Sox2 also interferes with Wnt signaling by binding to β-catenin, a central mediator of the Wnt pathway. We show that these functions of Sox2 are essential for mouse molar development. Sox2 has previously been shown to play a role in the formation of new teeth from the existing dental epithelium. To assess Sox2 function related to cell migration within a tooth, we monitored cell movement by using a DiI system and observed that DiI moves from molar 1 to molar 2 during tooth development. However, upon temporal knockdown of Sox2, DiI remains in the molar 1 region. This study also provides novel insights into the role of Sox2 and the important validation of Sox2 as a potent target in Wnt signaling during tooth development. Our data reveal that the degradation of Wnt signaling caused by the knockdown of Sox2 results in a lack of cell migration during tooth development.
Full Text
http://link.springer.com/article/10.1007/s00441-016-2363-4
DOI
10.1007/s00441-016-2363-4
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers
Yonsei Authors
Kim, Eun-Jung(김은정) ORCID logo https://orcid.org/0000-0002-9515-7590
Jung, Han Sung(정한성) ORCID logo https://orcid.org/0000-0003-2795-531X
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/147086
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