Sox2 contributes to tooth development via Wnt signaling
Sox2 contributes to tooth development via Wnt signaling
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DOI：
10.1007/s00441-016-2363-4
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发表时间：
2016-07-01
影响因子：
3.6
通讯作者：
Jung, Han-Sung
中科院分区：
文献类型：
--
作者：
Lee, Min-Jung;Kim, Eun-Jung;Jung, Han-Sung
转录因子 Sox2 是决定细胞谱系的干细胞标记。它已被证明可以标记持续生长的小鼠门牙的上皮干细胞。 Sox2 还通过与 Wnt 通路的中心介质 β-连环蛋白结合来干扰 Wnt 信号传导。我们证明 Sox2 的这些功能对于小鼠臼齿发育至关重要。 Sox2 先前已被证明在现有牙齿上皮形成新牙齿的过程中发挥作用。为了评估与牙齿内细胞迁移相关的 Sox2 功能，我们使用 DiI 系统监测细胞运动，并观察到 DiI 在牙齿发育过程中从 1 号臼齿移动到 2 号臼齿。然而，在暂时敲低 Sox2 后，DiI 仍保留在摩尔 1 区域。这项研究还为 Sox2 的作用提供了新的见解，并验证了 Sox2 作为牙齿发育过程中 Wnt 信号传导的有效靶标。我们的数据表明，Sox2 敲低引起的 Wnt 信号降解导致牙齿发育过程中细胞迁移的缺乏。
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 beta-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.