Reciprocal interactions of Fgf10/Fgfr2b modulate the mouse tongue epithelial differentiation

Sohn, Wern Joo; Jung, Hye In; Choi, Min A.; Han, Jin; Gwon, Gi Jeong; Yamamoto, Hitoshi; Lee, Sanggyu; Ryoo, Zae Young; Park, Eui Kyun; Shin, Hong In; Jung, Han Sung; Kim, Jae Young

doi:10.1007/s00441-011-1204-8

Cited by 6 publications

(3 citation statements)

References 36 publications

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“…Fgf7 is also expressed in the mesenchyme of the developing tongue and may compensate for the loss of Fgf10 in this structure (Sohn et al, 2011). These differences with the published data may indicate variation due to genetic background.…”

Section: Discussionmentioning

confidence: 99%

Multiple Cranial Organ Defects after Conditionally Knocking Out Fgf10 in the Neural Crest

2016

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Fgf10 is necessary for the development of a number of organs that fail to develop or are reduced in size in the null mutant. Here we have knocked out Fgf10 specifically in the neural crest driven by Wnt1cre. The Wnt1creFgf10fl/fl mouse phenocopies many of the null mutant defects, including cleft palate, loss of salivary glands, and ocular glands, highlighting the neural crest origin of the Fgf10 expressing mesenchyme surrounding these organs. In contrast tissues such as the limbs and lungs, where Fgf10 is expressed by the surrounding mesoderm, were unaffected, as was the pituitary gland where Fgf10 is expressed by the neuroepithelium. The circumvallate papilla of the tongue formed but was hypoplastic in the conditional and Fgf10 null embryos, suggesting that other sources of FGF can compensate in development of this structure. The tracheal cartilage rings showed normal patterning in the conditional knockout, indicating that the source of Fgf10 for this tissue is mesodermal, which was confirmed using Wnt1cre-dtTom to lineage trace the boundary of the neural crest in this region. The thyroid, thymus, and parathyroid glands surrounding the trachea were present but hypoplastic in the conditional mutant, indicating that a neighboring source of mesodermal Fgf10 might be able to partially compensate for loss of neural crest derived Fgf10.

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Section: Discussionmentioning

confidence: 99%

Multiple Cranial Organ Defects after Conditionally Knocking Out Fgf10 in the Neural Crest

2016

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“…The expression pattern of various Fibroblast Growth Factors (FGFs) and their receptors has been elucidated in the developing tongue ( Nie, 2005 ; Sohn et al, 2011 ; Du et al, 2016 ). Fgf10 is strongly expressed in the developing CVP mesenchyme, and Fgf10 knockout (KO) mice show a loss of the CVP phenotype ( Petersen et al, 2011 ).…”

Section: Introductionmentioning

confidence: 99%

FGF10 Is Required for Circumvallate Papilla Morphogenesis by Maintaining Lgr5 Activity

et al. 2018

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Taste buds develop in different regions of the mammal oral cavity. Adult stem cells in various organs including the tongue papillae are marked by leucine-rich repeat-containing G protein-coupled receptor 5 (Lgr5) and its homolog, Lgr6. Recent studies have reported that adult taste stem/progenitor cells in circumvallate papilla (CVP) on the posterior tongue are Lgr5-positive. In this study, we confirm the Lgr5 expression pattern during CVP development. A previous study reported that mesenchymal Fgf10 is necessary for maintaining epithelial Lgr5-positive stem/progenitor cells. To confirm the interaction between Lgr5-positive CVP epithelium and mesenchymal factor FGF10, reverse recombination (180-degree) was performed after tongue epithelium detachment. FGF10 protein-soaked bead implantation was performed after reverse recombination to rescue CVP development. Moreover, we reduced mesenchymal Fgf10 by BIO and SU5402 treatment which disrupted CVP morphogenesis. This study suggests that the crosstalk between epithelial Lgr5 and mesenchymal Fgf10 plays a pivotal role in CVP epithelium invagination during mouse tongue CVP development by maintaining Lgr5-positive stem/progenitor cells.

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“…A rolling organ culture system also has been used for mouse embryonic tongues on day 12.5 or 13.5 of gestation [ 29 , 30 ] ( Table 2 ). In this system, the tongues were cultured in medium containing various cytokines, antibodies, or enzyme inhibitors; thus, the effects of the molecules on the developing tongues could be precisely examined.…”

Section: Culture Of Lingual Epithelial Cellsmentioning

confidence: 99%

Lingual Epithelial Stem Cells and Organoid Culture of Them

Hisha

Tanaka

Ueno

2016

IJMS

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As tongue cancer is one of the major malignant cancers in the world, understanding the mechanism of maintenance of lingual epithelial tissue, which is known to be the origin of tongue cancer, is unquestionably important. However, the actual stem cells that are responsible for the long-term maintenance of the lingual epithelium have not been identified. Moreover, a simple and convenient culture method for lingual epithelial stem cells has not yet been established. Recently, we have shown that Bmi1-positive cells, residing at the second or third layer of the epithelial cell layer at the base of the interpapillary pit (IPP), were slow-cycling and could supply keratinized epithelial cells for over one year, indicating that Bmi1-positive cells are long-term lingual epithelial stem cells. In addition, we have developed a novel lingual epithelium organoid culture system using a three-dimensional matrix and growth factors. Here, we discuss current progress in the identification of lingual stem cells and future applications of the lingual culture system for studying the regulatory mechanisms of the lingual epithelium and for regenerative medicine.

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Reciprocal interactions of Fgf10/Fgfr2b modulate the mouse tongue epithelial differentiation

Cited by 6 publications

References 36 publications

Multiple Cranial Organ Defects after Conditionally Knocking Out Fgf10 in the Neural Crest

Multiple Cranial Organ Defects after Conditionally Knocking Out Fgf10 in the Neural Crest

FGF10 Is Required for Circumvallate Papilla Morphogenesis by Maintaining Lgr5 Activity

Lingual Epithelial Stem Cells and Organoid Culture of Them

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