Talk:Buccopharyngeal membrane

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On this website the Discussion Tab or "talk pages" for a topic has been used for several purposes: References - recent and historic that relates to the topic Additional topic information - currently prepared in draft format Links - to related webpages Topic page - an edit history as used on other Wiki sites Lecture/Practical - student feedback Student Projects - online project discussions. Links: Pubmed Most Recent | Reference Tutorial | Journal Searches Glossary Links Glossary: A | B | C | D | E | F | G | H | I | J | K | L | M | N | O | P | Q | R | S | T | U | V | W | X | Y | Z | Numbers | Symbols | Term Link Cite this page: Hill, M.A. (2024, April 23) Embryology Buccopharyngeal membrane. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Buccopharyngeal_membrane

2017

Mouth development

Wiley Interdiscip Rev Dev Biol. 2017 Sep;6(5). doi: 10.1002/wdev.275. Epub 2017 May 17.

Chen J1,2, Jacox LA1,3,4, Saldanha F1, Sive H1,2.

A mouth is present in all animals, and comprises an opening from the outside into the oral cavity and the beginnings of the digestive tract to allow eating. This review focuses on the earliest steps in mouth formation. In the first half, we conclude that the mouth arose once during evolution. In all animals, the mouth forms from ectoderm and endoderm. A direct association of oral ectoderm and digestive endoderm is present even in triploblastic animals, and in chordates, this region is known as the extreme anterior domain (EAD). Further support for a single origin of the mouth is a conserved set of genes that form a 'mouth gene program' including foxA and otx2. In the second half of this review, we discuss steps involved in vertebrate mouth formation, using the frog Xenopus as a model. The vertebrate mouth derives from oral ectoderm from the anterior neural ridge, pharyngeal endoderm and cranial neural crest (NC). Vertebrates form a mouth by breaking through the body covering in a precise sequence including specification of EAD ectoderm and endoderm as well as NC, formation of a 'pre-mouth array,' basement membrane dissolution, stomodeum formation, and buccopharyngeal membrane perforation. In Xenopus, the EAD is also a craniofacial organizer that guides NC, while reciprocally, the NC signals to the EAD to elicit its morphogenesis into a pre-mouth array. Human mouth anomalies are prevalent and are affected by genetic and environmental factors, with understanding guided in part by use of animal models. WIREs Dev Biol 2017, 6:e275. doi: 10.1002/wdev.275 For further resources related to this article, please visit the WIREs website.

© 2017 The Authors. WIREs Developmental Biology published by Wiley Periodicals, Inc.

PMID: 28514120 PMCID: PMC5574021 DOI: 10.1002/wdev.275

Role of JNK during buccopharyngeal membrane perforation, the last step of embryonic mouth formation

Dev Dyn. 2017 Feb;246(2):100-115. doi: 10.1002/dvdy.24470. Epub 2016 Dec 29.

Houssin NS1, Bharathan NK2, Turner SD3, Dickinson AJ1.

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.

© 2016 Wiley Periodicals, Inc.

KEYWORDS: JNK; buccopharyngeal membrane; embryonic mouth; intercellular adhesion PMID: 28032936 PMCID: PMC5261731 DOI: 10.1002/dvdy.24470

2013

Novel airway findings in a patient with 1p36 deletion syndrome

Int J Pediatr Otorhinolaryngol. 2014 Jan;78(1):157-8. doi: 10.1016/j.ijporl.2013.08.041. Epub 2013 Nov 14.

Ferril GR1, Barham HP2, Prager JD3.

1p36 deletion syndrome comprises a phenotypic presentation that includes central nervous system, cardiac, and craniofacial anomalies. There has been no report of associated airway anomalies with this syndrome. We present here a case report and literature review. Prenatally, amniocentesis for chromosomal analysis was performed on our patient, with results consistent with 1p36 deletion syndrome. Respiratory distress and unsuccessful attempts at intubation prompted transfer to Children's Hospital of Colorado. Microlaryngoscopy was subsequently performed, revealing a persistent buccopharyngeal membrane and unidentifiable larynx. Emergent tracheostomy was then performed to secure the airway. Airway anomalies may be associated with 1p36 deletion syndrome.

Published by Elsevier Ireland Ltd.

KEYWORDS: 1p36 deletion syndrome; Airway PMID: 24290305 DOI: 10.1016/j.ijporl.2013.08.041