The role of Hippo signaling in tooth development

Li, Chunhui; Li, Chang-Zhao

doi:10.1016/j.jfma.2015.03.011

Cited by 8 publications

(6 citation statements)

References 8 publications

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“…Tooth development is a multistage and multistep process involving fate determination and patterning events, epithelialmesenchymal interactions, and cell proliferation, differentiation, and migration (17) . In this study, cusps (14) .…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical Localization of YAP and TAZ in Mouse Molar Tooth Germ

2023

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Tooth development is a multistage and multistep process involving fate determination and morphogenetic patterning events, epithelialmesenchymal interactions, and cell proliferation, differentiation, and migration. Animal model studies have shown that YAP and TAZ, effectors of the Hippo pathway, have a critical function in tooth morphogenesis. However, the function of YAP and TAZ in tooth development has not been well documented and its specific roles in tooth morphogenesis remain unclear. We used immunohistochemistry to examine the localization of YAP and TAZ in mouse mandibular first molar tooth germ. ICR mouse embryos on days E12, E14 and E18 were produced.Heads from these embryos were processed for paraffin embedding and prepared for immunohistochemistry. Immunostaining for YAP and TAZ showed different localization in tooth development. YAP was localized in the odontogenic epithelium from the early stages of tooth germ, but TAZ was not almost observed. YAP was also positive for preameloblasts or inner enamel epithelium, which were high columnar cells. On the other hand, TAZ localized to odontoblasts and preameloblasts or inner enamel epithelium. These results demonstrated functional differences between YAP and TAZ in tooth development, and suggested that these proteins were not only involved in cell proliferation, differentiation, and hard tissue formation, but also in threedimensional cusp morphogenesis during tooth development.

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Section: Discussionmentioning

confidence: 99%

Immunohistochemical Localization of YAP and TAZ in Mouse Molar Tooth Germ

2023

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“…Differences in the phenotype caused by disruption of VPS4B in human and mouse might be explained by several mechanisms: (1) The different tooth development patterns. It is already known that mouse teeth are constantly growing, a phenomenon which continues throughout life [5]; however, humans have two sets of teeth: deciduous teeth and permanent teeth. At the time of tooth emergence, the root is not fully formed, the medullary cavity is large, and the apical hole is flared open.…”

Section: Discussionmentioning

confidence: 99%

“…Vacuolar protein sorting 4 (VPS4) is one of the major members of the ATP enzyme AAA protein family and is known to promote protein degradation and cell membrane fusion [1–3]. In humans, two homologues, VPS4A and VPS4B , both of which share 80% homology, have been identified [4, 5]. The gene encoding VPS4A is located on chromosome 16, while the gene encoding VPS4B is located on chromosome 18.…”

Section: Introductionmentioning

confidence: 99%

Vps4b heterozygous mice do not develop tooth defects that replicate human dentin dysplasia I

Lü

Chen

et al. 2019

BMC Genet

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BackgroundVacuolar protein sorting-associated protein 4B (VPS4B) is a member of the ATP enzyme AAA protein family, and is mainly involved in protein degradation and cell membrane fusion. Recently, a dominant mutation in this gene was identified in human dentin dysplasia type I (DD-I). Herein, we report the generation of Vps4b knockout (Vps4b KO) mice; however, the homozygous Vps4b KO mutation was embryonic lethal at the early stages of embryo development, and we therefore report the results of heterozygous mutant mice.ResultsMice heterozygous for Vps4b did not develop tooth defects replicating human DD-I. Immunohistochemistry showed that gene KO was successful, as there was decreased expression of Vps4b in heterozygous mice; hematoxylin and eosin (H&E) staining also showed that the width of the pre-dentin zone was increased in heterozygous mice, although the arrangement of the odontoblasts was not significantly different from wild-type (WT) mice. However, H&E staining showed no obvious abnormalities in the bones of heterozygous mice. Moreover, stereomicroscopic and X-ray radiography results indicated no abnormal manifestations in teeth or bones. Furthermore, statistical analysis of the volume and density of dentin and enamel, as well as skeletal analysis, including the volume and separation of trabecular bone analyzed by micro-CT, all showed no differences between Vps4b heterozygotes and WT mice. In addition, there also were no significant differences in bone or cartilage mineralization as evaluated by Alcian blue–Alizarin red staining.ConclusionsThe heterozygous Vps4b KO mice do not develop tooth defects that replicate human DD-I and this is likely to be due to differences in tooth development between the two species. Consequently, further studies are needed to determine whether mice are an appropriate animal model for human tooth diseases.

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“…LATS1 is a member of the hippo pathway known to control organ size; more recently, evidence suggests that the hippo pathway may also regulate tooth development. 53 According to DECIPHER, patients with chromosome abnormalities including the LATS1 gene have facial and dental anomalies; yet no asymmetric phenotypes have been described. BMP signaling regulates left to right patterning in mammalian development.…”

Section: Discussionmentioning

confidence: 99%

Candidate gene analyses of 3-dimensional dentoalveolar phenotypes in subjects with malocclusion

Weaver

Miller

Fontoura

et al. 2017

American Journal of Orthodontics and Dentofacial Orthopedics

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Introduction Genetic studies of malocclusion etiology have identified 4 deleterious mutations in genes, DUSP6, ARHGAP21, FGF23, and ADAMTS1 in familial Class III cases. Although these variants may have large impacts on Class III phenotypic expression, their low frequency (<1%) makes them unlikely to explain most malocclusions. Thus, much of the genetic variation underlying the dentofacial phenotypic variation associated with malocclusion remains unknown. In this study, we evaluated associations between common genetic variations in craniofacial candidate genes and 3-dimensional dentoalveolar phenotypes in patients with malocclusion. Methods Pretreatment dental casts or cone-beam computed tomographic images from 300 healthy subjects were digitized with 48 landmarks. The 3-dimensional coordinate data were submitted to a geometric morphometric approach along with principal component analysis to generate continuous phenotypes including symmetric and asymmetric components of dentoalveolar shape variation, fluctuating asymmetry, and size. The subjects were genotyped for 222 single-nucleotide polymorphisms in 82 genes/loci, and phenotpye-genotype associations were tested via multivariate linear regression. Results Principal component analysis of symmetric variation identified 4 components that explained 68% of the total variance and depicted anteroposterior, vertical, and transverse dentoalveolar discrepancies. Suggestive associations (P < 0.05) were identified with PITX2, SNAI3, 11q22.2-q22.3, 4p16.1, ISL1, and FGF8. Principal component analysis for asymmetric variations identified 4 components that explained 51% of the total variations and captured left-to-right discrepancies resulting in midline deviations, unilateral crossbites, and ectopic eruptions. Suggestive associations were found with TBX1 AJUBA, SNAI3 SATB2, TP63, and 1p22.1. Fluctuating asymmetry was associated with BMP3 and LATS1. Associations for SATB2 and BMP3 with asymmetric variations remained significant after the Bonferroni correction (P <0.00022). Suggestive associations were found for centroid size, a proxy for dentoalveolar size variation with 4p16.1 and SNAI1. Conclusions Specific genetic pathways associated with 3-dimensional dentoalveolar phenotypic variation in malocclusions were identified.

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The role of Hippo signaling in tooth development

Cited by 8 publications

References 8 publications

Immunohistochemical Localization of YAP and TAZ in Mouse Molar Tooth Germ

Immunohistochemical Localization of YAP and TAZ in Mouse Molar Tooth Germ

Vps4b heterozygous mice do not develop tooth defects that replicate human dentin dysplasia I

Candidate gene analyses of 3-dimensional dentoalveolar phenotypes in subjects with malocclusion

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