Publications by authors named "Cyril Charles"

Background: Unlike many vertebrates with continuous dental replacement, mammals have a maximum of two dental generations. Due to the absence of dental replacement in the laboratory mouse, the mechanisms of the mammalian tooth replacement system are poorly known. In this study, we use the European rabbit as a model for mammalian tooth development and replacement.

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Dental development mechanisms in mammals are highly studied using the mouse as a biological model. However, the mouse has a single, unreplaced, set of teeth. Features of mammalian tooth replacement are thus poorly known.

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FGF signaling plays a critical role in tooth development, and mutations in modulators of this pathway produce a number of striking phenotypes. However, many aspects of the role of the FGF pathway in regulating the morphological features and the mineral quality of the dentition remain unknown. Here, we used transgenic mice overexpressing the FGF negative feedback regulator Sprouty4 under the epithelial keratin 14 promoter (K14-) to achieve downregulation of signaling in the epithelium.

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Weaning practices differ among great apes and likely diverged during the course of human evolution, but behavioral inference from the fossil record is hampered by a lack of unambiguous biomarkers. Here, we show that early-life dietary transitions are recorded in human deciduous tooth enamel as marked variations in Ca isotope ratios (δCa). Using a sequential microsampling method along the enamel growth axis, we collected more than 150 enamel microsamples from 51 deciduous teeth of 12 different modern human individuals of known dietary histories, as well as nine enamel samples from permanent third molars.

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Luminescent core-shell crystals based on lanthanide tris-dipicolinate complexes were obtained from the successive growing of two different lanthanide complex layers. Selective or simultaneous emission of each part of the crystal can be achieved by a careful choice of the excitation wavelength.

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The question of phenotypic convergence across a signalling pathway has important implications for both developmental and evolutionary biology. The ERK-MAPK cascade is known to play a central role in dental development, but the relative roles of its components remain unknown. Here we investigate the diversity of dental phenotypes in Spry2(-/-), Spry4(-/-), and Rsk2(-/Y) mice, including the incidence of extra teeth, which were lost in the mouse lineage 45 million years ago (Ma).

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Mammalian dental morphology is under strong evolutionary pressure because of its importance for mastication and diet. While the mechanisms underlying tooth development have been widely studied in model organisms, the role of genetic regulatory elements in patterning the different elements of the occlusal surface and crown height across species is not well understood. Previous studies showed that Fibroblast Growth Factor (FGF) genes are important regulators of tooth development that influence morphological variation.

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We provide novel data on vertebral ontogeny in the mouse, the mammalian model-of-choice for developmental studies. Most previous studies on ossification sequences in mice have focused on pooled elements of the spine (cervicals, thoracics, lumbars, sacrals, and caudals). Here, we contribute data on ossification sequences in the neural arches and centra to provide a comparative basis upon which to evaluate mammalian diversity of the axial skeleton.

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Thyroid hormone (T3) is required for postnatal skeletal growth. It exerts its effect by binding to nuclear receptors, TRs including TRα1 and TRβ1, which are present in most cell types. These cell types include chondrocytes and osteoblasts, the interactions of which are known to regulate endochondral bone formation.

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Costello syndrome (CS) is a RASopathy characterized by a wide range of cardiac, musculoskeletal, dermatological, and developmental abnormalities. The RASopathies are defined as a group of syndromes caused by activated Ras/mitogen-activated protein kinase (MAPK) signaling. Specifically, CS is caused by activating mutations in HRAS.

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Adaptive radiations in mammals are sometimes associated with the emergence of key dental innovations facilitating food processing and masticatory movements. The dietary aspects of such innovations constitute an important focus in evolutionary biology. Murine rodents, which originated during middle Miocene, currently constitute the largest extant mammalian subfamily.

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RASopathies are syndromes caused by gain-of-function mutations in the Ras signaling pathway. One of these conditions, Costello syndrome (CS), is typically caused by an activating de novo germline mutation in HRAS and is characterized by a wide range of cardiac, musculoskeletal, dermatological and developmental abnormalities. We report that a majority of individuals with CS have hypo-mineralization of enamel, the outer covering of teeth, and that similar defects are present in a CS mouse model.

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In paleontology, many changes affecting morphology, such as tooth shape in mammals, are interpreted as ecological adaptations that reflect important selective events. Despite continuing studies, the identification of the genetic bases and key ecological drivers of specific mammalian dental morphologies remains elusive. Here we focus on the genetic and functional bases of stephanodonty, a pattern characterized by longitudinal crests on molars that arose in parallel during the diversification of murine rodents.

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The extant mammals have evolved highly diversified diets associated with many specialized morphologies. Two rare diets, termitophagy and vermivory, are characterized by unusual morphological and dental adaptations that have evolved independently in several clades. Termitophagy is known to be associated with increases in tooth number, crown simplification, enamel loss, and the appearance of intermolar diastemata.

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Dental characters are importantly used for reconstructing the evolutionary history of mammals, because teeth represent the most abundant material available for the fossil species. However, the characteristics of dental renewal are presently poorly used, probably because dental formulae are frequently not properly established, whereas they could be of high interest for evolutionary and developmental issues. One of the oldest rodent families, the Ctenodactylidae, is intriguing in having longstanding disputed dental formulae.

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Random chemical mutagenesis of the mouse genome can causally connect genes to specific phenotypes. Using this approach, reduced pinna (rep) or microtia, a defect in ear development, was mapped to a small region of mouse chromosome 2. Sequencing of this region established co-segregation of the phenotype (rep) with a mutation in the Prkra gene, which encodes the protein PACT/RAX.

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Much of our knowledge about mammalian evolution comes from examination of dental fossils, because the highly calcified enamel that covers teeth causes them to be among the best-preserved organs. As mammals entered new ecological niches, many changes in tooth number occurred, presumably as adaptations to new diets. For example, in contrast to humans, who have two incisors in each dental quadrant, rodents only have one incisor per quadrant.

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When it comes to mouse evo-devo, the fourth premolar-first molar (P4-M1) dental complex becomes a source of longstanding controversies among paleontologists and biologists. Muroidea possess only molar teeth but with additional mesial cusps on their M1. Developmental studies tend to demonstrate that the formation of such mesial cusps could result from the integration of a P4 germ into M1 during odontogenesis.

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The sense of taste is fundamental to our ability to ingest nutritious substances and to detect and avoid potentially toxic ones. Sensory taste buds are housed in papillae that develop from epithelial placodes. Three distinct types of gustatory papillae reside on the rodent tongue: small fungiform papillae are found in the anterior tongue, whereas the posterior tongue contains the larger foliate papillae and a single midline circumvallate papilla (CVP).

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Background: The fish order Cypriniformes is one of the most diverse ray-finned fish groups in the world with more than 3000 recognized species. Cypriniformes are characterized by a striking distribution of their dentition: namely the absence of oral teeth and presence of pharyngeal teeth on the last gill arch (fifth ceratobranchial). Despite this limited localisation, the diversity of tooth patterns in Cypriniformes is astonishing.

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A central challenge in evolutionary biology is understanding how genetic mutations underlie morphological changes. Because highly calcified enamel enables preservation of detailed dental features, studying tooth morphology enables this question to be addressed in both extinct and extant species. Previous studies have found that mutant mice can have severe abnormalities in tooth morphology, and several authors have explored the evolutionary implications of tooth number modifications in mutants.

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Changes in tooth shape have played a major role in vertebrate evolution with modification of dentition allowing an organism to adapt to new feeding strategies. The current view is that molar teeth evolved from simple conical teeth, similar to canines, by progressive addition of extra "cones" to form progressively complex multicuspid crowns. Mammalian incisors, however, are neither conical nor multicuspid, and their evolution is unclear.

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Background: The Eda-A1-Edar signaling pathway is involved in the development of organs with an ectodermal origin, including teeth. In mouse, mutants are known for both the ligand, Eda-A1 (Tabby), and the receptor, Edar (Downless). The adult dentitions of these two mutants have classically been considered to be similar.

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Background: The development of the secondary palate has been a main topic in craniofacial research, as its failure results in cleft palate, one of the most common birth defects in human. Nevertheless, palatal rugae (or rugae palatinae), which are transversal ridges developing on the secondary palate, received little attention. However, rugae could be useful as landmarks to monitor anterior/posterior (A/P) palatal growth, and they provide a simple model of mesenchymal-epithelial structures arranged in a serial pattern.

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The Tabby/eda mice, which bear a loss of function mutation for the eda (ectodysplasinA) gene, are known to display developmental anomalies in organs with an ectodermal origin. Although the lower jugal (cheek) teeth of Tabby/eda mice have been extensively studied, upper teeth have never been investigated in detail. However, this may help us to further understand the function of the eda gene in tooth development.

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