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Sox2通过Wnt信号通路促进牙齿发育。

Sox2 contributes to tooth development via Wnt signaling.

作者信息

Lee Min-Jung, Kim Eun-Jung, Otsu Keishi, Harada Hidemitsu, Jung Han-Sung

机构信息

Division in Anatomy and Developmental Biology, Department of Oral Biology, Oral Science Research Center, BK21 PLUS Project, Yonsei University College of Dentistry, 50-1 Yonsei-ro, Seodaemoon-Gu, Seoul, 03722, South Korea.

Division of Developmental Biology and Regenerative Medicine, Department of Anatomy, Iwate Medical University, Yahaba, Japan.

出版信息

Cell Tissue Res. 2016 Jul;365(1):77-84. doi: 10.1007/s00441-016-2363-4. Epub 2016 Feb 4.

DOI:10.1007/s00441-016-2363-4
PMID:26846112
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.

摘要

转录因子Sox2是一种决定细胞谱系的干细胞标志物。它已被证明可标记持续生长的小鼠门齿的上皮干细胞。Sox2还通过与β-连环蛋白(Wnt信号通路的核心介质)结合来干扰Wnt信号传导。我们发现Sox2的这些功能对小鼠磨牙发育至关重要。此前已表明Sox2在由现存牙上皮形成新牙的过程中发挥作用。为评估Sox2与牙齿内细胞迁移相关的功能,我们使用DiI系统监测细胞运动,并观察到在牙齿发育过程中DiI从第一磨牙迁移至第二磨牙。然而,在短暂敲低Sox2后,DiI仍留在第一磨牙区域。本研究还为Sox2的作用提供了新见解,并对Sox2作为牙齿发育过程中Wnt信号传导的有效靶点进行了重要验证。我们的数据表明,敲低Sox2导致的Wnt信号传导降解会致使牙齿发育过程中细胞迁移缺失。

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