Expression of Sox genes in tooth development

Kawasaki, Keisuke; Kawasaki, Maiko; Watanabe, Momoko; Idrus, Erik; Nagai, Takahiro; Oommen, Shelly; Maeda, Takeyasu; Hagiwara, Nobuko; Que, Jianwen; Sharpe, Paul T.; Ohazama, Atsushi

doi:10.1387/ijdb.150192ao

Cited by 24 publications

(19 citation statements)

References 31 publications

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“…3K), whereas in the Sox2 CreERT2/+ ; Ctnnb1 lox(ex3) embryos Sox9 was expressed in the forming successional tooth (Fig. 3L), in a similar pattern to that previously described for Sox9 at the cap stage (Kawasaki et al, 2015).…”

Section: Resultssupporting

confidence: 78%

Revitalising the rudimentary replacement dentition in the mouse

2019

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Most mammals have two sets of teeth (diphyodont)a deciduous dentition replaced by a permanent dentition; however, the mouse possesses only one tooth generation (monophyodont). In diphyodonts, the replacement tooth forms on the lingual side of the first tooth from the successional dental lamina. This lamina expresses the stem/progenitor marker Sox2 and has activated Wnt/β-catenin signalling at its tip. Although the mouse does not replace its teeth, a transient rudimentary successional dental lamina (RSDL) still forms during development. The mouse RSDL houses Sox2-positive cells, but no Wnt/β-catenin signalling. Here, we show that stabilising Wnt/ β-catenin signalling in the RSDL in the mouse leads to proliferation of the RSDL and formation of lingually positioned teeth. Although Sox2 has been shown to repress Wnt activity, overexpression of Wnts leads to a downregulation of Sox2, suggesting a negative-feedback loop in the tooth. In the mouse, the first tooth represses the formation of the replacement, and isolation of the RSDL is sufficient to induce formation of a new tooth germ. Our data highlight key mechanisms that may have influenced the evolution of replacement teeth. This article has an associated 'The people behind the papers' interview.

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Section: Resultssupporting

confidence: 78%

Revitalising the rudimentary replacement dentition in the mouse

2019

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“…In addition, it has been reported that the target genes of miR-499-5p in the anti-apoptosis process of myocardial cells may be PDCD4, calcineurin (CaN) and promoter protein-related protein-1 (Drp-1) (Chua et al 2016 ; Jia et al 2016 ; Wang et al 2011 ). SOX6 plays a crucial role in cell and organ development (Kawasaki et al 2015 ; Panman et al 2014 ). Studies have confirmed that miR-499-5p induced the up-regulation of type-I fiber number by inhibiting SOX6 (van Rooij et al 2009 ).…”

Section: Discussionmentioning

confidence: 99%

MiR-499 inhibited hypoxia/reoxygenation induced cardiomyocytes injury by targeting SOX6

Shi

Yun-feng²,

Niu³

et al. 2019

Biotechnol Lett

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Objective MiR-499 has been reported to be expressed only in cardiomyocytes, and its expression would increase after acute myocardial infarction (AMI). miR-499 plays a role in the process of cardiomyocytes injury induced by hypoxia/reoxygenation (H/R), however, it still remains unclear. Results Hypoxia inhibited miR-499-5p expression and H/R induced apoptosis. SOX6 was a target gene of miR-499-5p, and high expression of miR-499-5p inhibited the expression of SOX6. MiR-499-5p reduced H9c2 cells injury by inhibiting the expression of SOX6, overexpression of which could reverse the effect of miR-499-5p on H9c2 cells. MiR-499-5p inhibited the levels of LDH and MDA, while overexpression of miR-499-5p inhibited H/R-induced cell apoptosis. MiR-499-5p could up-regulate the level of Bcl-2 and down-regulate the expression levels of Bax and caspase-3. However, SOX6 partially reversed these effects of miR-499-5p. Conclusion We proved that miR-499-5p inhibited H/R-induced cardiomyocytes injury by targeting SOX6. Our results suggested that miR-499-5p/SOX6 pathway may present a potential therapeutic target for the treatment of AMI.

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“…n/a n/a n/a n/a More detailed expression patterns for factors can be found in: (Kawasaki et al, 2015;Watanabe et al, 2016;Ishikawa et al, 2018). Epithelial (Epi), Mesenchymal (Mes), Muscle (Mus), Not expressed (n.e).…”

Section: G Sox15mentioning

confidence: 99%

Sorting Sox: Diverse Roles for Sox Transcription Factors During Neural Crest and Craniofacial Development

Schock

LaBonne

2020

Front. Physiol.

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Sox transcription factors play many diverse roles during development, including regulating stem cell states, directing differentiation, and influencing the local chromatin landscape. Of the twenty vertebrate Sox factors, several play critical roles in the development the neural crest, a key vertebrate innovation, and the subsequent formation of neural crest-derived structures, including the craniofacial complex. Herein, we review the specific roles for individual Sox factors during neural crest cell formation and discuss how some factors may have been essential for the evolution of the neural crest. Additionally, we describe how Sox factors direct neural crest cell differentiation into diverse lineages such as melanocytes, glia, and cartilage and detail their involvement in the development of specific craniofacial structures. Finally, we highlight several SOXopathies associated with craniofacial phenotypes.

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Expression of Sox genes in tooth development

Cited by 24 publications

References 31 publications

Revitalising the rudimentary replacement dentition in the mouse

Revitalising the rudimentary replacement dentition in the mouse

MiR-499 inhibited hypoxia/reoxygenation induced cardiomyocytes injury by targeting SOX6

Sorting Sox: Diverse Roles for Sox Transcription Factors During Neural Crest and Craniofacial Development

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