Sox21 Regulates Anapc10 Expression and Determines the Fate of Ectodermal Organ
Summary: The transcription factor Sox21 is expressed in the epithelium of developing teeth. The present study aimed to determine the role of Sox21 in tooth development. We found that disruption of Sox21 caused severe enamel hypoplasia, regional osteoporosis, and ectopic hair formation in the gingiva...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Kan Saito [verfasserIn] Frederic Michon [verfasserIn] Aya Yamada [verfasserIn] Hiroyuki Inuzuka [verfasserIn] Satoko Yamaguchi [verfasserIn] Emiko Fukumoto [verfasserIn] Keigo Yoshizaki [verfasserIn] Takashi Nakamura [verfasserIn] Makiko Arakaki [verfasserIn] Yuta Chiba [verfasserIn] Masaki Ishikawa [verfasserIn] Hideyuki Okano [verfasserIn] Irma Thesleff [verfasserIn] Satoshi Fukumoto [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2020 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
In: iScience - Elsevier, 2019, 23(2020), 7, Seite 101329- |
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| Übergeordnetes Werk: |
volume:23 ; year:2020 ; number:7 ; pages:101329- |
| Links: |
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| DOI / URN: |
10.1016/j.isci.2020.101329 |
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| Katalog-ID: |
DOAJ007298269 |
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| 245 | 1 | 0 | |a Sox21 Regulates Anapc10 Expression and Determines the Fate of Ectodermal Organ |
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| 520 | |a Summary: The transcription factor Sox21 is expressed in the epithelium of developing teeth. The present study aimed to determine the role of Sox21 in tooth development. We found that disruption of Sox21 caused severe enamel hypoplasia, regional osteoporosis, and ectopic hair formation in the gingiva in Sox21 knockout incisors. Differentiation markers were lost in ameloblasts, which formed hair follicles expressing hair keratins. Molecular analysis and chromatin immunoprecipitation sequencing indicated that Sox21 regulated Anapc10, which recognizes substrates for ubiquitination-mediated degradation, and determined dental-epithelial versus hair follicle cell fate. Disruption of either Sox21 or Anapc10 induced Smad3 expression, accelerated TGF-β1-induced promotion of epithelial-to-mesenchymal transition (EMT), and resulted in E-cadherin degradation via Skp2. We conclude that Sox21 disruption in the dental epithelium leads to the formation of a unique microenvironment promoting hair formation and that Sox21 controls dental epithelial differentiation and enamel formation by inhibiting EMT via Anapc10. | ||
| 650 | 4 | |a Rodent Dentistry | |
| 650 | 4 | |a Developmental Genetics | |
| 650 | 4 | |a Transcriptomics | |
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| 700 | 0 | |a Aya Yamada |e verfasserin |4 aut | |
| 700 | 0 | |a Hiroyuki Inuzuka |e verfasserin |4 aut | |
| 700 | 0 | |a Satoko Yamaguchi |e verfasserin |4 aut | |
| 700 | 0 | |a Emiko Fukumoto |e verfasserin |4 aut | |
| 700 | 0 | |a Keigo Yoshizaki |e verfasserin |4 aut | |
| 700 | 0 | |a Takashi Nakamura |e verfasserin |4 aut | |
| 700 | 0 | |a Makiko Arakaki |e verfasserin |4 aut | |
| 700 | 0 | |a Yuta Chiba |e verfasserin |4 aut | |
| 700 | 0 | |a Masaki Ishikawa |e verfasserin |4 aut | |
| 700 | 0 | |a Hideyuki Okano |e verfasserin |4 aut | |
| 700 | 0 | |a Irma Thesleff |e verfasserin |4 aut | |
| 700 | 0 | |a Satoshi Fukumoto |e verfasserin |4 aut | |
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10.1016/j.isci.2020.101329 doi (DE-627)DOAJ007298269 (DE-599)DOAJb8f5cb3372324ed98382e503ff281643 DE-627 ger DE-627 rakwb eng Kan Saito verfasserin aut Sox21 Regulates Anapc10 Expression and Determines the Fate of Ectodermal Organ 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: The transcription factor Sox21 is expressed in the epithelium of developing teeth. The present study aimed to determine the role of Sox21 in tooth development. We found that disruption of Sox21 caused severe enamel hypoplasia, regional osteoporosis, and ectopic hair formation in the gingiva in Sox21 knockout incisors. Differentiation markers were lost in ameloblasts, which formed hair follicles expressing hair keratins. Molecular analysis and chromatin immunoprecipitation sequencing indicated that Sox21 regulated Anapc10, which recognizes substrates for ubiquitination-mediated degradation, and determined dental-epithelial versus hair follicle cell fate. Disruption of either Sox21 or Anapc10 induced Smad3 expression, accelerated TGF-β1-induced promotion of epithelial-to-mesenchymal transition (EMT), and resulted in E-cadherin degradation via Skp2. We conclude that Sox21 disruption in the dental epithelium leads to the formation of a unique microenvironment promoting hair formation and that Sox21 controls dental epithelial differentiation and enamel formation by inhibiting EMT via Anapc10. Rodent Dentistry Developmental Genetics Transcriptomics Science Q Frederic Michon verfasserin aut Aya Yamada verfasserin aut Hiroyuki Inuzuka verfasserin aut Satoko Yamaguchi verfasserin aut Emiko Fukumoto verfasserin aut Keigo Yoshizaki verfasserin aut Takashi Nakamura verfasserin aut Makiko Arakaki verfasserin aut Yuta Chiba verfasserin aut Masaki Ishikawa verfasserin aut Hideyuki Okano verfasserin aut Irma Thesleff verfasserin aut Satoshi Fukumoto verfasserin aut In iScience Elsevier, 2019 23(2020), 7, Seite 101329- (DE-627)1019532106 25890042 nnns volume:23 year:2020 number:7 pages:101329- https://doi.org/10.1016/j.isci.2020.101329 kostenfrei https://doaj.org/article/b8f5cb3372324ed98382e503ff281643 kostenfrei http://www.sciencedirect.com/science/article/pii/S2589004220305162 kostenfrei https://doaj.org/toc/2589-0042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 23 2020 7 101329- |
| spelling |
10.1016/j.isci.2020.101329 doi (DE-627)DOAJ007298269 (DE-599)DOAJb8f5cb3372324ed98382e503ff281643 DE-627 ger DE-627 rakwb eng Kan Saito verfasserin aut Sox21 Regulates Anapc10 Expression and Determines the Fate of Ectodermal Organ 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: The transcription factor Sox21 is expressed in the epithelium of developing teeth. The present study aimed to determine the role of Sox21 in tooth development. We found that disruption of Sox21 caused severe enamel hypoplasia, regional osteoporosis, and ectopic hair formation in the gingiva in Sox21 knockout incisors. Differentiation markers were lost in ameloblasts, which formed hair follicles expressing hair keratins. Molecular analysis and chromatin immunoprecipitation sequencing indicated that Sox21 regulated Anapc10, which recognizes substrates for ubiquitination-mediated degradation, and determined dental-epithelial versus hair follicle cell fate. Disruption of either Sox21 or Anapc10 induced Smad3 expression, accelerated TGF-β1-induced promotion of epithelial-to-mesenchymal transition (EMT), and resulted in E-cadherin degradation via Skp2. We conclude that Sox21 disruption in the dental epithelium leads to the formation of a unique microenvironment promoting hair formation and that Sox21 controls dental epithelial differentiation and enamel formation by inhibiting EMT via Anapc10. Rodent Dentistry Developmental Genetics Transcriptomics Science Q Frederic Michon verfasserin aut Aya Yamada verfasserin aut Hiroyuki Inuzuka verfasserin aut Satoko Yamaguchi verfasserin aut Emiko Fukumoto verfasserin aut Keigo Yoshizaki verfasserin aut Takashi Nakamura verfasserin aut Makiko Arakaki verfasserin aut Yuta Chiba verfasserin aut Masaki Ishikawa verfasserin aut Hideyuki Okano verfasserin aut Irma Thesleff verfasserin aut Satoshi Fukumoto verfasserin aut In iScience Elsevier, 2019 23(2020), 7, Seite 101329- (DE-627)1019532106 25890042 nnns volume:23 year:2020 number:7 pages:101329- https://doi.org/10.1016/j.isci.2020.101329 kostenfrei https://doaj.org/article/b8f5cb3372324ed98382e503ff281643 kostenfrei http://www.sciencedirect.com/science/article/pii/S2589004220305162 kostenfrei https://doaj.org/toc/2589-0042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 23 2020 7 101329- |
| allfields_unstemmed |
10.1016/j.isci.2020.101329 doi (DE-627)DOAJ007298269 (DE-599)DOAJb8f5cb3372324ed98382e503ff281643 DE-627 ger DE-627 rakwb eng Kan Saito verfasserin aut Sox21 Regulates Anapc10 Expression and Determines the Fate of Ectodermal Organ 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: The transcription factor Sox21 is expressed in the epithelium of developing teeth. The present study aimed to determine the role of Sox21 in tooth development. We found that disruption of Sox21 caused severe enamel hypoplasia, regional osteoporosis, and ectopic hair formation in the gingiva in Sox21 knockout incisors. Differentiation markers were lost in ameloblasts, which formed hair follicles expressing hair keratins. Molecular analysis and chromatin immunoprecipitation sequencing indicated that Sox21 regulated Anapc10, which recognizes substrates for ubiquitination-mediated degradation, and determined dental-epithelial versus hair follicle cell fate. Disruption of either Sox21 or Anapc10 induced Smad3 expression, accelerated TGF-β1-induced promotion of epithelial-to-mesenchymal transition (EMT), and resulted in E-cadherin degradation via Skp2. We conclude that Sox21 disruption in the dental epithelium leads to the formation of a unique microenvironment promoting hair formation and that Sox21 controls dental epithelial differentiation and enamel formation by inhibiting EMT via Anapc10. Rodent Dentistry Developmental Genetics Transcriptomics Science Q Frederic Michon verfasserin aut Aya Yamada verfasserin aut Hiroyuki Inuzuka verfasserin aut Satoko Yamaguchi verfasserin aut Emiko Fukumoto verfasserin aut Keigo Yoshizaki verfasserin aut Takashi Nakamura verfasserin aut Makiko Arakaki verfasserin aut Yuta Chiba verfasserin aut Masaki Ishikawa verfasserin aut Hideyuki Okano verfasserin aut Irma Thesleff verfasserin aut Satoshi Fukumoto verfasserin aut In iScience Elsevier, 2019 23(2020), 7, Seite 101329- (DE-627)1019532106 25890042 nnns volume:23 year:2020 number:7 pages:101329- https://doi.org/10.1016/j.isci.2020.101329 kostenfrei https://doaj.org/article/b8f5cb3372324ed98382e503ff281643 kostenfrei http://www.sciencedirect.com/science/article/pii/S2589004220305162 kostenfrei https://doaj.org/toc/2589-0042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 23 2020 7 101329- |
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10.1016/j.isci.2020.101329 doi (DE-627)DOAJ007298269 (DE-599)DOAJb8f5cb3372324ed98382e503ff281643 DE-627 ger DE-627 rakwb eng Kan Saito verfasserin aut Sox21 Regulates Anapc10 Expression and Determines the Fate of Ectodermal Organ 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: The transcription factor Sox21 is expressed in the epithelium of developing teeth. The present study aimed to determine the role of Sox21 in tooth development. We found that disruption of Sox21 caused severe enamel hypoplasia, regional osteoporosis, and ectopic hair formation in the gingiva in Sox21 knockout incisors. Differentiation markers were lost in ameloblasts, which formed hair follicles expressing hair keratins. Molecular analysis and chromatin immunoprecipitation sequencing indicated that Sox21 regulated Anapc10, which recognizes substrates for ubiquitination-mediated degradation, and determined dental-epithelial versus hair follicle cell fate. Disruption of either Sox21 or Anapc10 induced Smad3 expression, accelerated TGF-β1-induced promotion of epithelial-to-mesenchymal transition (EMT), and resulted in E-cadherin degradation via Skp2. We conclude that Sox21 disruption in the dental epithelium leads to the formation of a unique microenvironment promoting hair formation and that Sox21 controls dental epithelial differentiation and enamel formation by inhibiting EMT via Anapc10. Rodent Dentistry Developmental Genetics Transcriptomics Science Q Frederic Michon verfasserin aut Aya Yamada verfasserin aut Hiroyuki Inuzuka verfasserin aut Satoko Yamaguchi verfasserin aut Emiko Fukumoto verfasserin aut Keigo Yoshizaki verfasserin aut Takashi Nakamura verfasserin aut Makiko Arakaki verfasserin aut Yuta Chiba verfasserin aut Masaki Ishikawa verfasserin aut Hideyuki Okano verfasserin aut Irma Thesleff verfasserin aut Satoshi Fukumoto verfasserin aut In iScience Elsevier, 2019 23(2020), 7, Seite 101329- (DE-627)1019532106 25890042 nnns volume:23 year:2020 number:7 pages:101329- https://doi.org/10.1016/j.isci.2020.101329 kostenfrei https://doaj.org/article/b8f5cb3372324ed98382e503ff281643 kostenfrei http://www.sciencedirect.com/science/article/pii/S2589004220305162 kostenfrei https://doaj.org/toc/2589-0042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 23 2020 7 101329- |
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10.1016/j.isci.2020.101329 doi (DE-627)DOAJ007298269 (DE-599)DOAJb8f5cb3372324ed98382e503ff281643 DE-627 ger DE-627 rakwb eng Kan Saito verfasserin aut Sox21 Regulates Anapc10 Expression and Determines the Fate of Ectodermal Organ 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: The transcription factor Sox21 is expressed in the epithelium of developing teeth. The present study aimed to determine the role of Sox21 in tooth development. We found that disruption of Sox21 caused severe enamel hypoplasia, regional osteoporosis, and ectopic hair formation in the gingiva in Sox21 knockout incisors. Differentiation markers were lost in ameloblasts, which formed hair follicles expressing hair keratins. Molecular analysis and chromatin immunoprecipitation sequencing indicated that Sox21 regulated Anapc10, which recognizes substrates for ubiquitination-mediated degradation, and determined dental-epithelial versus hair follicle cell fate. Disruption of either Sox21 or Anapc10 induced Smad3 expression, accelerated TGF-β1-induced promotion of epithelial-to-mesenchymal transition (EMT), and resulted in E-cadherin degradation via Skp2. We conclude that Sox21 disruption in the dental epithelium leads to the formation of a unique microenvironment promoting hair formation and that Sox21 controls dental epithelial differentiation and enamel formation by inhibiting EMT via Anapc10. Rodent Dentistry Developmental Genetics Transcriptomics Science Q Frederic Michon verfasserin aut Aya Yamada verfasserin aut Hiroyuki Inuzuka verfasserin aut Satoko Yamaguchi verfasserin aut Emiko Fukumoto verfasserin aut Keigo Yoshizaki verfasserin aut Takashi Nakamura verfasserin aut Makiko Arakaki verfasserin aut Yuta Chiba verfasserin aut Masaki Ishikawa verfasserin aut Hideyuki Okano verfasserin aut Irma Thesleff verfasserin aut Satoshi Fukumoto verfasserin aut In iScience Elsevier, 2019 23(2020), 7, Seite 101329- (DE-627)1019532106 25890042 nnns volume:23 year:2020 number:7 pages:101329- https://doi.org/10.1016/j.isci.2020.101329 kostenfrei https://doaj.org/article/b8f5cb3372324ed98382e503ff281643 kostenfrei http://www.sciencedirect.com/science/article/pii/S2589004220305162 kostenfrei https://doaj.org/toc/2589-0042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 23 2020 7 101329- |
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Sox21 Regulates Anapc10 Expression and Determines the Fate of Ectodermal Organ Rodent Dentistry Developmental Genetics Transcriptomics |
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Kan Saito Frederic Michon Aya Yamada Hiroyuki Inuzuka Satoko Yamaguchi Emiko Fukumoto Keigo Yoshizaki Takashi Nakamura Makiko Arakaki Yuta Chiba Masaki Ishikawa Hideyuki Okano Irma Thesleff Satoshi Fukumoto |
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sox21 regulates anapc10 expression and determines the fate of ectodermal organ |
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Sox21 Regulates Anapc10 Expression and Determines the Fate of Ectodermal Organ |
| abstract |
Summary: The transcription factor Sox21 is expressed in the epithelium of developing teeth. The present study aimed to determine the role of Sox21 in tooth development. We found that disruption of Sox21 caused severe enamel hypoplasia, regional osteoporosis, and ectopic hair formation in the gingiva in Sox21 knockout incisors. Differentiation markers were lost in ameloblasts, which formed hair follicles expressing hair keratins. Molecular analysis and chromatin immunoprecipitation sequencing indicated that Sox21 regulated Anapc10, which recognizes substrates for ubiquitination-mediated degradation, and determined dental-epithelial versus hair follicle cell fate. Disruption of either Sox21 or Anapc10 induced Smad3 expression, accelerated TGF-β1-induced promotion of epithelial-to-mesenchymal transition (EMT), and resulted in E-cadherin degradation via Skp2. We conclude that Sox21 disruption in the dental epithelium leads to the formation of a unique microenvironment promoting hair formation and that Sox21 controls dental epithelial differentiation and enamel formation by inhibiting EMT via Anapc10. |
| abstractGer |
Summary: The transcription factor Sox21 is expressed in the epithelium of developing teeth. The present study aimed to determine the role of Sox21 in tooth development. We found that disruption of Sox21 caused severe enamel hypoplasia, regional osteoporosis, and ectopic hair formation in the gingiva in Sox21 knockout incisors. Differentiation markers were lost in ameloblasts, which formed hair follicles expressing hair keratins. Molecular analysis and chromatin immunoprecipitation sequencing indicated that Sox21 regulated Anapc10, which recognizes substrates for ubiquitination-mediated degradation, and determined dental-epithelial versus hair follicle cell fate. Disruption of either Sox21 or Anapc10 induced Smad3 expression, accelerated TGF-β1-induced promotion of epithelial-to-mesenchymal transition (EMT), and resulted in E-cadherin degradation via Skp2. We conclude that Sox21 disruption in the dental epithelium leads to the formation of a unique microenvironment promoting hair formation and that Sox21 controls dental epithelial differentiation and enamel formation by inhibiting EMT via Anapc10. |
| abstract_unstemmed |
Summary: The transcription factor Sox21 is expressed in the epithelium of developing teeth. The present study aimed to determine the role of Sox21 in tooth development. We found that disruption of Sox21 caused severe enamel hypoplasia, regional osteoporosis, and ectopic hair formation in the gingiva in Sox21 knockout incisors. Differentiation markers were lost in ameloblasts, which formed hair follicles expressing hair keratins. Molecular analysis and chromatin immunoprecipitation sequencing indicated that Sox21 regulated Anapc10, which recognizes substrates for ubiquitination-mediated degradation, and determined dental-epithelial versus hair follicle cell fate. Disruption of either Sox21 or Anapc10 induced Smad3 expression, accelerated TGF-β1-induced promotion of epithelial-to-mesenchymal transition (EMT), and resulted in E-cadherin degradation via Skp2. We conclude that Sox21 disruption in the dental epithelium leads to the formation of a unique microenvironment promoting hair formation and that Sox21 controls dental epithelial differentiation and enamel formation by inhibiting EMT via Anapc10. |
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Sox21 Regulates Anapc10 Expression and Determines the Fate of Ectodermal Organ |
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