Gsk3β is required in the epithelium for palatal elevation in mice.
Gsk3β is required in the epithelium for palatal elevation in mice.
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DOI：
10.1002/dvdy.22466
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发表时间：
2010-12
影响因子：
2.5
通讯作者：
Chen, Yiping
中科院分区：
文献类型：
--
作者：
He, Fenglei;Popkie, Anthony P.;Xiong, Wei;Li, Lu;Wang, Ying;Phiel, Christopher J.;Chen, Yiping
在Wnt/β-catenin信号通路中，Gsk 3 β的功能是促进β-catenin的降解。小鼠Gsk 3 β失活导致腭裂形成，提示Wnt/β-catenin信号通路参与了腭裂的形成。本研究探讨了Gsk 3 β在小鼠腭发育过程中的表达模式、组织特异性需求及其功能。我们发现Gsk 3 β主要表达于腭上皮，特别是与β-catenin重叠的内侧缘上皮（medial edge epithelium，EEP）。组织特异性基因失活研究表明，Gsk 3 β在上腭隆起上皮中起重要作用，Gsk 3 β突变体中Gsk 3 β的破坏有助于腭裂表型。我们观察到Aixn 2的表达，Wnt/β-catenin信号的直接靶基因，在突变舌中异位激活，但在腭中不激活。我们的研究结果表明，Gsk 3 β是腭部发育所需的上皮细胞的内在调节因子，并且可以通过不依赖于Wnt/β-catenin信号传导的途径来调节腭部发育。
In Wnt/β-catenin signaling pathway, Gsk3β functions to facilitate β-catenin degradation. Inactivation of Gsk3β in mice causes a cleft palate formation, suggesting an involvement of Wnt/β-catenin signaling during palatogenesis. In this study, we have investigated the expression pattern, tissue-specific requirement and function of Gsk3β during mouse palatogenesis. We showed that Gsk3β is primarily expressed in the palatal epithelium, particularly in the medial edge epithelium (MEE) overlapping with β-catenin. Tissue-specific gene inactivation studies demonstrated an essential role for Gsk3β in the epithelium for palate elevation, and disruption of which contributes to cleft palate phenotype in Gsk3β mutant. We observed that expression of Aixn2, a direct target gene of Wnt/β-catenin signaling, is ectopically activated in the mutant tongue, but not in the palate. Our results indicate that Gsk3β is an intrinsic regulator required in the epithelium for palate elevation, and could act through a pathway independent of Wnt/β-catenin signaling to regulate palate development.
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