Mouth development

Abstract

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.275For further resources related to this article, please visit the WIREs website.

Programmed Cell Death Not as Sledgehammer but as Chisel: Apoptosis in Normal and Abnormal Craniofacial Patterning and Development

“…Apoptosis-associated apposition may also be basalbasal in nature wherein initial contact between epithelial sheets occurs along their basal lamina and basement membranes. This is typified by the apposition of the PE and the SCE, such as at the buccopharyngeal membrane and the PPts (Watermann, 1977;Shone and Graham, 2014;Chen et al, 2017).…”

“…After significant intranasal epithelial morphogenesis, coupled with differential proliferation of the underlying CNC, an oronasal membrane composed of two SCE-derived epithelial sheets with apposing basement membranes separates the oral and nasal cavities (Tamarin, 1982). Rupture of this membrane is essential for the tetrapodal ability to breath with the mouth closed, proceeds without cell intercalation, and is accompanied by apoptotic cells at the site of disintegration (Weingaertner et al, 2006;Chen et al, 2017). Here, again, apoptosis appears to play a more surgical role than an obliterative one.…”

Identification of Isthmin 1 as a Novel Clefting and Craniofacial Patterning Gene in Humans

“…Due to the high conservation of orofacial development between humans and Xenopus and the well-established use of Xenopus as a model organism, this vertebrate has become an effective model to study orofacial development and defects (Dickinson and Sive 2006;Dickinson 2016;Chen et al 2017;Dubey and Saint-Jeannet 2017). Elegant bead implantation and transplantation studies in Xenopus from the Sive laboratory have helped characterize specific cellular mechanisms involved in craniofacial development, including the role of the Kinin-Kallikrein and Wnt/planar cell polarity pathways in mouth formation (Jacox et al 2014(Jacox et al , 2016.…”

The Influence of Brain-Skull Interactions on the Development of the Amphibian Skull

“…This results in malformed palatine and maxillary bones. While the existence of the FEZ is uncertain in Xenopus, its development in chick and mouse involves expression of Fgf8 and Shh, two genes that are critical for facial development in Xenopus (Chen et al, 2017). Further investigation of the role of the forebrain in Xenopus facial skeleton primordia patterning will provide valuable information for the connection between facial development in poorly-known early-diverging tetrapods.…”

“…The inability for the cartilage to complete growth to its final destination is possibly due to reduced Fgf8 signaling (Anderson, 1997;Eagleson and Dempewolf, 2002). Although the exact role of Shh and Fgf8 expression in chondrogenesis has not yet been determined in Xenopus, it is known that both Shh and Fgf8 are expressed in the anterior domain of the head and interruption of their expression can lead to craniofacial abnormalities (Chen et al, 2017). As Fgf8 and Shh signaling has been thoroughly studied in chick and mouse, it will be important to determine what similarities are shared by amphibians.…”