Journal of Oral Biosciences最新文献

{"title":"Solute carrier family 9 member A5 regulated by TGF-β is necessary for dental enamel formation","authors":"Hayato Takano ,&nbsp;Risako Chiba-Ohkuma ,&nbsp;Saeko Kobayashi ,&nbsp;Ryuji Yamamoto ,&nbsp;Rei Kataoka ,&nbsp;Yuri Miyakawa ,&nbsp;Yoshinobu Asada ,&nbsp;Yasuo Yamakoshi","doi":"10.1016/j.job.2025.100719","DOIUrl":"10.1016/j.job.2025.100719","url":null,"abstract":"<div><h3>Objectives</h3><div>In this study, we aimed to elucidate the functional significance of transforming growth factor-β (TGF-β)-regulated SLC9A5 (NHE5) in enamel formation.</div></div><div><h3>Methods</h3><div>Mouse ameloblast-derived mHAT9d cells were treated with TGF-β1, TGF-β2, or TGF-β3, and the expression of <em>Slc9a</em> family members was analyzed via RNA sequencing (RNA-seq) and quantitative PCR (qPCR). <em>Slc9a5</em>-deficient mice were generated to examine enamel morphology. Enamel volume, mineral density, and structure were assessed using micro-computed tomography (μCT), scanning electron microscopy (SEM), and electron probe microanalysis (EPMA). Protein expression was analyzed via SDS–PAGE, western blotting, and immunohistochemistry.</div></div><div><h3>Results</h3><div>RNA-seq and qPCR analyses revealed that TGF-β1 and TGF-β3 strongly induced <em>Slc9a5</em> in a dose-dependent manner; however, TGF-β2 had a minimal effect. In <em>Slc9a5</em>-deficient mice, incomplete crown formation and pit-like defects were evident on postnatal day 5; however, enamel protein profiles and thickness formation at day 11 were comparable to those in wild-type mice. In contrast, by day 70, μCT revealed marked thinning of enamel and reduced mineral density, SEM showed cracks and surface defects, and EPMA demonstrated significantly lower calcium-to-phosphorus (Ca/P) molar ratios than in wild-type mice. These findings indicate that loss of <em>Slc9a5</em> slightly affects protein secretion but causes defective mineral maturation and enamel fragility.</div></div><div><h3>Conclusions</h3><div><em>SLC9A5</em> is a downstream target of TGF-β signaling, which is indispensable for enamel maturation because it maintains ion transport and extracellular pH homeostasis in ameloblasts. Its deficiency leads to reduced mineral density, altered Ca/P composition, and progressive enamel loss. These findings underscore the essential role of <em>SLC9A5</em> in the long-term structural stability of enamel.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100719"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145690961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of Mycobacterium-derived plasmids for application in oral Actinomyces species","authors":"Sakiko Ohara ,&nbsp;Yijuan Sheng ,&nbsp;Yuki Nishiya ,&nbsp;Ikue Tosa ,&nbsp;Katsuki Takebe ,&nbsp;Yuki Arimura ,&nbsp;Hiroshi Mese ,&nbsp;Naoko Ohara ,&nbsp;Naoya Ohara","doi":"10.1016/j.job.2025.100718","DOIUrl":"10.1016/j.job.2025.100718","url":null,"abstract":"<div><h3>Objectives</h3><div>Genetic manipulation tools are essential for elucidating the pathogenic mechanisms of microorganisms. Several species of <em>Actinomyces,</em> including <em>A</em>. <em>israelii,</em> are present in the oral cavity and they are the causative agents of actinomycosis. However, efficient gene-editing tools for these species have not yet been developed. In this study, the aim was to evaluate the introduction of foreign genes into <em>Actinomyces</em> using plasmids derived from <em>Mycobacterium</em>, which belong to the same class as <em>Actinomycetes</em>.</div></div><div><h3>Methods</h3><div>A truncated derivative of pYT923, pYT923S, which contains the replication origin of the <em>M</em>. <em>scrofulaceum</em> plasmid pMSC262 was constructed and introduced into <em>A. israelii</em> by electrotransformation.</div></div><div><h3>Results</h3><div>pYT923S was successfully introduced into <em>A. israelii</em>. The transformation efficiency of <em>A. israelii</em> was approximately 7–66 CFU/μg of DNA, and all transformed colonies harbored pYT923S. The plasmid recovered from <em>A. israelii</em> replicated in <em>Escherichia coli</em>.</div></div><div><h3>Conclusions</h3><div>pYT923S was introduced into and maintained within <em>A. israelii</em>. Therefore, the pYT923S vector represents a useful genetic tool for <em>Actinomyces</em> and it is expected to facilitate future studies on the biology and pathogenicity of <em>Actinomyces</em>.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100718"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145691039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Odontogenic ameloblast-associated protein (ODAM)-enriched coating improves adhesion of junctional epithelial cells to composite resin via AKT activation","authors":"Masayoshi Takaman ,&nbsp;Keishi Otsu ,&nbsp;Shojiro Ikezaki ,&nbsp;Mamoru Noda ,&nbsp;Hidemitsu Harada","doi":"10.1016/j.job.2025.100725","DOIUrl":"10.1016/j.job.2025.100725","url":null,"abstract":"<div><h3>Objectives</h3><div>Although the junctional epithelium (JE) forms a biological seal around the teeth, attachment is often unstable in cases of subgingival extension of the composite resin (CR) margins. Odontogenic ameloblast-associated protein (ODAM), a JE-specific extracellular matrix protein, regulates adhesion and cytoskeletal dynamics. This study investigated whether an ODAM-enriched coating on CR surfaces enhances JE cell function, and elucidated the underlying molecular mechanisms.</div></div><div><h3>Methods</h3><div>An ODAM-enriched fraction was purified and coated onto CR discs. The mHAT-JE01 cells were cultured on either uncoated or ODAM-coated surfaces. Cell adhesion and proliferation were assessed by fluorescence imaging and Ki67 staining, cell migration by wound healing, and cell morphology by scanning electron microscopy. The expression of focal adhesion–related molecules, actin filaments, and phosphorylated AKT was analyzed using immunofluorescence and quantitative polymerase chain reaction. An AKT inhibitor was used to evaluate the need for AKT signaling.</div></div><div><h3>Results</h3><div>ODAM coating of CR surfaces significantly enhanced the adhesion, proliferation, and migration of JE cells, reinforcing actin stress fibers, promoting vinculin accumulation at the cell periphery and protrusions, and increasing phosphorylated AKT levels. ODAM coating induced its own expression, suggesting a novel positive feedback mechanism that amplifies the biological effects. AKT inhibition suppressed ODAM-mediated changes, confirming that AKT is the central hub for focal adhesion–related signaling and epithelial responses.</div></div><div><h3>Conclusions</h3><div>These findings support the role of ODAM as a bioactive molecule that contributes to subgingival margin stabilization, mitigates peri-restorative inflammation, and enhances long-term periodontal and restorative outcomes.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100725"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145796677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insights into the taste of organic acids via TAS1Rs","authors":"Yuko Yamase ,&nbsp;Katsuki Takebe ,&nbsp;Kengo Horie ,&nbsp;Yoshihiro Mitoh ,&nbsp;Atsuko Yamashita ,&nbsp;Ryusuke Yoshida","doi":"10.1016/j.job.2025.100731","DOIUrl":"10.1016/j.job.2025.100731","url":null,"abstract":"<div><h3>Objectives</h3><div>Organic acids contribute significantly to the flavor of fermented foods by imparting sourness. Although mice generally avoid sour taste, previous studies have reported greater consumption of <span>l</span>-lactic acid than its <span>d</span>-enantiomer, suggesting enantiomer-specific recognition. This behavior is hypothesized to involve TAS1Rs, which consists of sweet/umami receptors. However, it remains unclear whether TAS1Rs additionally contribute to the recognition of other chiral organic acids. This study aimed to evaluate the role of TAS1Rs, particularly TAS1R3, in the modulation of enantiomer-dependent behavioral responses to organic acids in mice.</div></div><div><h3>Methods</h3><div>Behavioral responses were evaluated using 48-h and 1-h 2-bottle tests. Binding of organic acids to TAS1Rs was investigated by differential scanning fluorimetry (DSF) with the ligand-binding domain (LBD) of medaka Tas1r2a/Tas1r3.</div></div><div><h3>Results</h3><div>Wild-type mice consumed more <span>d</span>-malic acid than <span>l</span>-malic acid in the 48-h test, whereas <em>Tas1r3</em>-KO mice showed no such difference. This pattern was not observed in the short-term 1-h test, which minimized the contribution of post-ingestion and learned effects. DSF analysis revealed no binding of any of the tested organic acids to the LBD of medaka Tas1r2a/Tas1r3.</div></div><div><h3>Conclusions</h3><div>Organic acids may elicit TAS1R3-dependent post-ingestion signals that contribute to enantiomer-selective consumption in mice. Electrostatic interactions and hydrogen-bonding networks within the orthosteric pocket of TAS1Rs may account for the differences in binding affinity to the LBD of medaka Tas1r2a/Tas1r3 between organic acids and L-alanine, a known ligand.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100731"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145938324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Propionic and acetic acids potentially compromise junctional epithelial barrier function and contribute to periodontitis progression","authors":"Takako Oikawa ,&nbsp;Toshitaka Miura ,&nbsp;Ting Wang ,&nbsp;Takashi Yaegashi ,&nbsp;Taichi Ishikawa ,&nbsp;Daisuke Sasaki","doi":"10.1016/j.job.2025.100716","DOIUrl":"10.1016/j.job.2025.100716","url":null,"abstract":"<div><h3>Objectives</h3><div>Periodontitis, a leading cause of tooth loss, is driven by pathogenic bacteria through classical virulence factors, including lipopolysaccharides, fimbriae, and proteases, and metabolic products such as short-chain fatty acids (SCFAs). Among these, butyric acid (BA) and lactic acid (LA) impair proliferation, migration, and inflammatory responses of gingival or junctional epithelial cells. However, the effects of other SCFAs, particularly propionic acid (PA) and acetic acid (AA), on the junctional epithelium remain unclear. In this study, the effects of PA and AA on murine JE-1 cells derived from the gingival junctional epithelium were examined.</div></div><div><h3>Methods</h3><div>JE-1 cells were treated with PA or AA. Wound healing, proliferation, viability, and cell cycle distribution were evaluated. The mRNA expression of adhesion molecules and cell cycle regulators was analyzed using quantitative reverse-transcription polymerase chain reaction.</div></div><div><h3>Results</h3><div>PA and AA markedly delayed wound closure and inhibited cell proliferation, without affecting cell viability. Both acids downregulated <em>Integrin α6</em> and <em>Integrin β4</em>, induced G0/G1 arrest, decreased <em>Ccnd1</em> expression<em>,</em> and increased <em>p21</em> expression.</div></div><div><h3>Conclusions</h3><div>PA and AA impair wound repair, proliferation, and adhesion of junctional epithelial cells by altering the progression of the cell cycle and expression of adhesion-related genes. Together with prior findings on BA and LA, these results indicate that multiple SCFAs from periodontopathic bacteria contribute to weakening of the epithelial barrier, in vitro, highlighting the requirement for <em>in viv</em>o studies to confirm their roles in the pathogenesis of periodontitis.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100716"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145580407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modeling GABAergic hyperexcitability in sleep bruxism patient-derived brainstem neurons using a multielectrode array platform","authors":"Mayu Onishi ,&nbsp;Akihiro Yamaguchi ,&nbsp;Yuka Abe ,&nbsp;Taro Sato ,&nbsp;Miho Fujishima ,&nbsp;Wado Akamatsu ,&nbsp;Kazuyoshi Baba","doi":"10.1016/j.job.2026.100743","DOIUrl":"10.1016/j.job.2026.100743","url":null,"abstract":"<div><h3>Objectives</h3><div>Sleep bruxism (SB) involves involuntary jaw movements during sleep and has been linked to impaired inhibitory regulation of brainstem circuits (particularly those involving GABAergic neurons). While previous studies using patch-clamp electrophysiology have demonstrated intrinsic hyperexcitability in neurons differentiated from SB patient-derived human induced pluripotent stem cells (hiPSCs), the low-throughput nature of this technique limits large-scale phenotypic screening. We aimed to establish a robust, high-throughput, multielectrode array (MEA)-based platform capable of quantitatively assessing electrophysiological phenotypes of SB-derived neurons.</div></div><div><h3>Methods</h3><div>hiPSCs from three patients with SB and three healthy controls were differentiated to become ventral brainstem-like neurons. Their neuronal composition was evaluated using immunocytochemistry for total neurons (TUBB3⁺) and GABAergic neurons (GAD1/2⁺). Spontaneous neuronal firing was assessed using MEA under steady-state conditions and immediately after medium change. Extracellular GABA levels were quantified via ELISA to indirectly assess GABAergic hyperexcitability.</div></div><div><h3>Results</h3><div>Differentiation efficiency to TUBB3⁺ or GAD1/2⁺ neurons did not differ among cell lines. Under steady-state conditions, the weighted mean firing rate (wMFR) did not differ between groups. The SB group showed significantly elevated extracellular GABA concentrations and a significant increase in wMFR immediately after medium change (GABA removal), suggesting that GABA hypersecretion concealed the underlying hyperexcitability of SB-derived neurons.</div></div><div><h3>Conclusions</h3><div>We developed a robust, high-throughput MEA platform that reliably quantifies SB-related electrophysiological phenotypes. Our findings indicate that SB-derived GABAergic neurons exhibit constitutive hyperexcitability and excessive GABA release, providing mechanistic insights and a scalable framework for therapeutic discovery.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100743"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146090692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intracellular mechanisms underlying modulation of inhibitory synaptic transmission by appetite-related peptides in the insular cortex","authors":"Yuka Nakaya ,&nbsp;Masayuki Kobayashi","doi":"10.1016/j.job.2025.100706","DOIUrl":"10.1016/j.job.2025.100706","url":null,"abstract":"<div><h3>Background</h3><div>The insular cortex (IC) integrates multimodal sensory inputs, including gustatory, visceral, nociceptive, and oral somatosensory information, and is widely regarded as the primary gustatory cortex. These functions are closely associated with feeding behaviors such as mastication, swallowing, and digestion, which are affected by appetite- and energy balance-related peptides.</div></div><div><h3>Highlight</h3><div>Orexin, leptin, and insulin have received particular attention because of their effects on IC circuits. Orexin, produced in the hypothalamus, activates postsynaptic phospholipase C, thereby inducing IP₃ and elevating intracellular calcium levels. This effect facilitates inhibitory transmission to pyramidal neurons and promotes an excitatory drive onto interneurons. Leptin, secreted by adipocytes, facilitates inhibitory transmission from fast-spiking interneurons to pyramidal neurons via the presynaptic JAK2–PI3K–Akt signaling pathway. Similarly, insulin increases GABA release from fast spiking interneurons to pyramidal neurons in a PI3K–Akt-dependent manner. This collective peptidergic modulation leads to a net facilitation of inhibition within IC circuits, potentially reducing cortical excitability and output.</div></div><div><h3>Conclusions</h3><div>Given the involvement of the IC in the processing of sensory, interoceptive, and reward-related information, this peptidergic regulation likely influences a range of behaviors, including feeding, pain perception, and addiction. Elucidating these intricate mechanisms could facilitate the development of novel therapeutic interventions for disorders such as obesity, chronic pain, and substance dependence.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100706"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145493015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New insights into the influence of surface roughness of titanium and zirconia-based materials in the regenerative behavior of human gingival keratinocytes","authors":"Irati Fernandez-de-Mendiola ,&nbsp;Igor Irastorza ,&nbsp;Sara Martin-Iglesias ,&nbsp;Gaskon Ibarretxe ,&nbsp;Fernando-José Unda ,&nbsp;Raphael S. Wagner ,&nbsp;Unai Silvan ,&nbsp;Lucía Jiménez-Rojo","doi":"10.1016/j.job.2025.100712","DOIUrl":"10.1016/j.job.2025.100712","url":null,"abstract":"<div><h3>Objectives</h3><div>This study aimed to investigate the impact of implant composition and surface modifications on the behavior of human gingival keratinocytes, a natural source of peri-implant epithelium.</div></div><div><h3>Methods</h3><div>The materials used in this study were titanium grade 4 and 3 mol% yttria-stabilized tetragonal zirconia polycrystal (3Y-TZP) discs with various surface modifications (e.g., polished, machined, sandblasted, and/or acid-etched). Surface roughness and wettability were first characterized, followed by culturing human gingival keratinocytes on these substrates. Cell morphology, adhesion, extracellular matrix (ECM) synthesis, cell cycle progression, and differentiation were analyzed using immunofluorescence and quantitative polymerase chain reaction (qPCR).</div></div><div><h3>Results</h3><div>The chemical composition and surface topography of the materials markedly influenced keratinocyte behavior. Specifically, reduced surface roughness enhanced the formation of mature focal adhesions, increased laminin-332 deposition, and promoted keratinocyte motility and proliferation. After 24 h of culture, smooth surfaces showed higher cell densities and a greater proportion of cycling cells. Interestingly, after one week of culture, smooth ceramic materials presented significantly higher gingival keratinocyte densities than smooth titanium surfaces. Furthermore, zirconia-based ceramic surfaces induced the expression of junctional epithelial markers, including keratin 19 (<em>KRT19</em>) and odontogenic ameloblast-associated protein (<em>ODAM</em>), while maintaining keratin 14 (<em>KRT14</em>) expression.</div></div><div><h3>Conclusions</h3><div>Our results demonstrate that biomaterials with smooth surfaces, especially of zirconia, induce pro-regenerative biological responses conducive to the development of a functional peri-implant epithelium.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100712"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145747945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identifying cell-type-specific marker genes of dental epithelial cells using single-cell RNA sequence: A review","authors":"Triana Marchelina ,&nbsp;Yuta Chiba ,&nbsp;Keigo Yoshizaki ,&nbsp;Satoshi Fukumoto","doi":"10.1016/j.job.2026.100757","DOIUrl":"10.1016/j.job.2026.100757","url":null,"abstract":"<div><h3>Background</h3><div>Single-cell RNA sequencing (scRNA-seq) has transformed our understanding of dental epithelial heterogeneity, revealing that dental cell types have distinct gene expression profiles. Ameloblasts differentiate from the inner enamel epithelium into the pre-ameloblast, secretory, and maturation phases, and their molecular functions have been extensively described. In contrast, the molecular markers and functional roles of non-ameloblast populations such as the outer enamel epithelium, stellate reticulum, and stratum intermedium, remain unexplored.</div></div><div><h3>Highlight</h3><div>We systematically compiled the canonical and newly proposed marker genes from published scRNA-seq tooth development studies. We integrated these datasets with experimental validations from the literature using immunostaining or <em>in situ</em> hybridization of mouse tooth tissues. We examined the dental phenotypes reported in mouse knockout models using the Mouse Genome Informatics and Online Mendelian Inheritance in Man databases to determine the functional relevance of each gene. Genes specifically expressed within each cluster validated by histological experiments, were further assessed using cap analysis of the gene expression sequencing (CAGE-seq) database in the mouse tooth germ and whole body to identify genes that were preferentially enriched in the teeth.</div></div><div><h3>Conclusion</h3><div>We established an updated molecular map for each dental epithelial cell type through integrating scRNA-seq, histological validation, phenotypic databases, and CAGE-seq. This framework describes the molecular identities of ameloblast and nonameloblast lineages, emphasizes key marker genes across dental epithelial populations, and provides a comprehensive basis for interpreting enamel phenotypes, guiding future tooth development research.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100757"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146187303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lineage tracing of Twist2-expressing cells in mouse taste buds","authors":"Namiki Takaku-Tanoue ,&nbsp;Kae Matsuyama ,&nbsp;Takashi Toyono ,&nbsp;Shinji Kataoka ,&nbsp;Mitsushiro Nakatomi ,&nbsp;Shingo Takai ,&nbsp;Noriatsu Shigemura ,&nbsp;Tatsuo Kawamoto ,&nbsp;Yuji Seta","doi":"10.1016/j.job.2025.100729","DOIUrl":"10.1016/j.job.2025.100729","url":null,"abstract":"<div><h3>Objectives</h3><div>It is widely accepted that Taste bud cells originate from the epithelium; however, evidence indicates that these cells are also derived from the mesenchyme beneath the epithelium. In this study, the cell lineage expressing <em>Twist2</em>, a transcription factor that is specifically expressed in the mesenchyme within taste buds, were examined to gain a deeper understanding of its biological characteristics.</div></div><div><h3>Methods</h3><div>Immunohistochemical analyses and taste organoid cultures were performed using <em>Twist2</em> lineage-tracing reporter mice (<em>Twist2-Cre</em> mice crossed with <em>tdTomato</em> mice) to identify <em>Twist2</em>-derived cells in taste buds. The transgenic mice were harvested at 7, 14, and 21 days, post-administration of 5-ethynyl-2′-deoxyuridine (EdU), to assess the label retention of <em>Twist2</em>-derived cells.</div></div><div><h3>Results</h3><div>tdTomato-positive cells expressed Type III taste cell markers in the taste papillae and soft palate. tdTomato-positive organoids derived from the circumvallate papilla contained numerous taste bud cells. EdU analysis revealed that tdTomato-positive cells expressing a Type III taste cell marker persisted for longer than tdTomato-negative cells that expressed the same marker. In addition, almost all the long-term cultured tdTomato-positive organoids contained cells expressing a Type II taste cell marker.</div></div><div><h3>Conclusions</h3><div>The findings support the hypothesis that mesenchymal cells contribute to the taste bud cell population.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100729"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145883339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}