Palatogenesis

Lévi, Benjamin; Brugman, Samantha; Wong, Victor W.; Grova, Monica; Longaker, Michael T.; Wan, Derrick C.

doi:10.4161/org.7.4.17926

Cited by 40 publications

(31 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In humans, development of the face begins in the fourth week of embryogenesis with migrating neural crest cells that combine with mesodermal and ectodermal cells to establish the facial primordia, which initially consist of five separate parts surrounding the primitive mouth, the stomodeum (reviewed by Jiang et al, 2006; Dixon et al, 2011; Levi et al, 2011). At the rostral midline is the frontonasal prominence, which is populated by mesenchymal cells derived from the forebrain and midbrain neural crest cells.…”

Section: Introductionmentioning

confidence: 99%

Cellular and Molecular Mechanisms of Palatogenesis

Lan

Jiang

2015

Current Topics in Developmental Biology

100

120

View full text Add to dashboard Cite

Palatogenesis involves the initiation, growth, morphogenesis, and fusion of the primary and secondary palatal shelves from initially separate facial prominences during embryogenesis to form the intact palate separating the oral cavity from the nostrils. The palatal shelves consist mainly of cranial neural crest-derived mesenchyme cells covered under a simple embryonic epithelium. Growth and patterning of the palatal shelves are controlled by reciprocal epithelial-mesenchymal interactions regulated by multiple signaling pathways and transcription factors. During palatal shelf outgrowth, the embryonic epithelium develops a “teflon” coat consisting of a single, continuous layer of periderm cells that prevents the facial prominences and palatal shelves from forming aberrant inter-epithelial adhesions. Palatal fusion involves not only spatiotemporally-regulated disruption of the periderm but also dynamic cellular and molecular processes that result in adhesion and intercalation of the palatal medial edge epithelia to form an inter-shelf epithelial seam, and subsequent dissolution of the epithelial seam to form the intact roof of the oral cavity. The complexity of regulation of these morphogenetic processes is reflected by the common occurrence of cleft palate in humans. This review will summarize major recent advances and discuss major remaining gaps in the understanding of cellular and molecular mechanisms controlling palatogenesis.

show abstract

Section: Introductionmentioning

confidence: 99%

Cellular and Molecular Mechanisms of Palatogenesis

Lan

Jiang

2015

Current Topics in Developmental Biology

100

120

View full text Add to dashboard Cite

show abstract

“…In this review, we summarize recent progress on how growth factor signaling contributes to neural crest differentiation and to skull morphology. Due to limited space, we will not mention palatogenesis, another important craniofacial developmental process where neural crest cells play critical roles [4–6]. …”

Section: Introductionmentioning

confidence: 99%

Neural crest cell signaling pathways critical to cranial bone development and pathology

Mishina

Snider

2014

Experimental Cell Research

View full text Add to dashboard Cite

Neural crest cells appear early during embryogenesis and give rise to many structures in the mature adult. In particular, a specific population of neural crest cells migrates to and populates developing cranial tissues. The ensuing differentiation of these cells via individually complex and often intersecting signaling pathways is indispensible to growth and development of the craniofacial complex. Much research has been devoted to this area of development with particular emphasis on cell signaling events required for physiologic development. Understanding such mechanisms will allow researchers to investigate ways in which they can be exploited in order to treat a multitude of diseases affecting the craniofacial complex. Knowing how these multipotent cells are driven towards distinct fates could, in due course, allow patients to receive regenerative therapies for tissues lost to a variety of pathologies. In order to realize this goal, nucleotide sequencing advances allowing snapshots of entire genomes and exomes are being utilized to identify molecular entities associated with disease states. Once identified, these entities can be validated for biological significance with other methods. A crucial next step is the integration of knowledge gleaned from observations in disease states with normal physiology to generate an explanatory model for craniofacial development. This review seeks to provide a current view of the landscape on cell signaling and fate determination of the neural crest and to provide possible avenues of approach for future research.

show abstract

“…9 Better understanding of the genetic basis of palate and cleft formation would aid genetic diagnosis of orofacial clefts and lead to potential advances in the treatment of these common structural malformations. 10–12 …”

mentioning

confidence: 99%

Functional Analysis of SPECC1L in Craniofacial Development and Oblique Facial Cleft Pathogenesis

Gfrerer

Shubinets

Hoyos

et al. 2014

Plastic and Reconstructive Surgery

View full text Add to dashboard Cite

Background Oblique facial clefts, also known as Tessier clefts, are severe orofacial clefts, the genetic basis of which is poorly understood. Human genetics studies revealed that disruption in SPECC1L resulted in oblique facial clefts, demonstrating that oblique facial cleft malformation has a genetic basis. An important step toward innovation in treatment of oblique facial clefts would be improved understanding of its genetic pathogenesis. The authors exploit the zebrafish model to elucidate the function of SPECC1L by studying its homolog, specc1lb. Methods Gene and protein expression analysis was carried out by reverse-transcriptase polymerase chain reaction and immunohistochemistry staining. Morpholino knockdown, mRNA rescue, lineage tracing and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assays were performed for functional analysis. Results Expression of specc1lb was detected in epithelia juxtaposed to chondrocytes. Knockdown of specc1lb resulted in bilateral clefts between median and lateral elements of the ethmoid plate, structures analogous to the frontonasal process and the paired maxillary processes. Lineage tracing analysis revealed that cranial neural crest cells contributing to the frontonasal prominence failed to integrate with the maxillary prominence populations. Cells contributing to lower jaw structures were able to migrate to their destined pharyngeal segment but failed to converge to form mandibular elements. Conclusions These results demonstrate that specc1lb is required for integration of frontonasal and maxillary elements and convergence of mandibular prominences. The authors confirm the role of SPECC1L in orofacial cleft pathogenesis in the first animal model of Tessier cleft, providing morphogenetic insight into the mechanisms of normal craniofacial development and oblique facial cleft pathogenesis.

show abstract

Palatogenesis

Cited by 40 publications

References 67 publications

Cellular and Molecular Mechanisms of Palatogenesis

Cellular and Molecular Mechanisms of Palatogenesis

Neural crest cell signaling pathways critical to cranial bone development and pathology

Functional Analysis of SPECC1L in Craniofacial Development and Oblique Facial Cleft Pathogenesis

Contact Info

Product

Resources

About