Role of JNK during buccopharyngeal membrane perforation, the last step of embryonic mouth formation.
Role of JNK during buccopharyngeal membrane perforation, the last step of embryonic mouth formation.
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JNK 在胚胎口腔形成的最后一步——颊咽膜穿孔过程中的作用。
DOI：
10.1002/dvdy.24470
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发表时间：
2017
期刊：
影响因子：
--
通讯作者：
Dickinson,AmandaJG
中科院分区：
文献类型：
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作者：
Houssin,NathalieS;Bharathan,NavaneethaKrishnan;Turner,StephenD;Dickinson,AmandaJG
背景：颊咽膜是覆盖在胚胎口腔上的一层薄层细胞。这个结构的穿孔形成了一个连接外部和消化管的开口，这对口腔的形成是必不可少的。在人类中，颊咽膜的持续存在可导致口腔面部缺陷，如后鼻孔闭锁、口腔粘连和腭裂。结果：利用反义和药理学方法，我们已经确定c-jun氨基末端激酶(JNK)信号通路缺陷的非洲爪哇胚胎具有持久的颊咽膜。JNK基因缺陷的胚胎细胞分裂减少，细胞应激和细胞凋亡增加。然而，独立于JNK改变这些突起并不影响颊咽膜穿孔。JNK缺陷胚胎还增加了细胞间黏附和e-钙粘附素定位缺陷。相反，JNK活性过高的胚胎具有表皮脆性，E-钙粘附素内化增加，膜定位的网状蛋白增加。在颊咽膜中，胞膜蛋白与活性JNK共定位。此外，抑制内吞作用会导致持久的颊咽膜，类似于JNK缺失的表型。结论：本研究结果表明，JNK在颊咽膜穿孔所需的内吞作用中参与了黏附连接的拆解。发育动力学246：100-115,2017。©2016 Wiley期刊，Inc.
Background:The buccopharyngeal membrane is a thin layer of cells covering the embryonic mouth. The perforation of this structure creates an opening connecting the external and the digestive tube which is essential for oral cavity formation. In humans, persistence of the buccopharyngeal membrane can lead to orofacial defects such as choanal atresia, oral synechiaes, and cleft palate. Little is known about the causes of a persistent buccopharyngeal membrane and, importantly, how this structure ruptures.Results: We have determined, using antisense and pharmacological approaches, thatXenopusembryos deficient c‐Jun N‐terminal kinase (JNK) signaling have a persistent buccopharyngeal membrane. JNK deficient embryos have decreased cell division and increased cellular stress and apoptosis. However, altering these processes independently of JNK did not affect buccopharyngeal membrane perforation. JNK deficient embryos also have increased intercellular adhesion and defects in e‐cadherin localization. Conversely, embryos with overactive JNK have epidermal fragility, increased E‐cadherin internalization, and increased membrane localized clathrin. In the buccopharyngeal membrane, clathrin is colocalized with active JNK. Furthermore, inhibition of endocytosis results in a persistent buccopharyngeal membrane, mimicking the JNK deficient phenotype.Conclusions:The results of this study suggest that JNK has a role in the disassembly adherens junctions by means of endocytosis that is required during buccopharyngeal membrane perforation.Developmental Dynamics 246:100–115, 2017. © 2016 Wiley Periodicals, Inc.