Role of JNK during buccopharyngeal membrane perforation, the last step of embryonic mouth formation. Issue 2 (29th December 2016)

• Record Type: Journal Article
• Authors: Houssin, Nathalie S.; Bharathan, Navaneetha Krishnan; Turner, Stephen D.; Dickinson, Amanda J.G.
• Is Part Of: Developmental dynamics. Volume 246:Issue 2(2017)
• Page Start: 100
• Page End: 115
• Publication Date: 2016-12-29
• Subjects: buccopharyngeal membrane -- embryonic mouth -- JNK -- intercellular adhesion; Morphogenesis -- Periodicals; Anatomy -- Periodicals; Anatomie -- Périodiques; Biologie du développement -- Périodiques; 571.833
• DOI: 10.1002/dvdy.24470
• Languages: English
• ISSNs: 1058-8388

Abstract

Abstract : 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, that Xenopus embryos 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. Key Findings: Decreased JNK signals cause a persistent buccopharyngeal membrane Decreased JNK signals cause decreased cell proliferation and increased cell death and oxidative stress but these problems do not cause a persistent buccopharyngeal membrane. JNK signals regulate intercellular adhesion in the epidermis and the buccopharyngeal membrane.