Canonical Wnt signaling is not required for Tgfb3 expression in the basal medial edge epithelium during palatogenesis
The secondary palate forms from two lateral primordia called the palatal shelves which form a contact in the midline, become adherent at the fusing interface (medial edge epithelia, MEE) and subsequently fuse. The gene encoding transforming growth factor-ß3 (Tgfb3) is strongly and specifically expre...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2023-05-01
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| Series: | Frontiers in Physiology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fphys.2023.704406/full |
| _version_ | 1797828995340828672 |
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| author | Ghazi-Abdullah Saroya Erica Siismets Erica Siismets Max Hu Max Hu Christopher Panaretos Adam Rice Kurt Reynolds Kurt Reynolds Chengji J. Zhou Chengji J. Zhou Vesa Kaartinen |
| author_facet | Ghazi-Abdullah Saroya Erica Siismets Erica Siismets Max Hu Max Hu Christopher Panaretos Adam Rice Kurt Reynolds Kurt Reynolds Chengji J. Zhou Chengji J. Zhou Vesa Kaartinen |
| author_sort | Ghazi-Abdullah Saroya |
| collection | DOAJ |
| description | The secondary palate forms from two lateral primordia called the palatal shelves which form a contact in the midline, become adherent at the fusing interface (medial edge epithelia, MEE) and subsequently fuse. The gene encoding transforming growth factor-ß3 (Tgfb3) is strongly and specifically expressed in MEE cells. Our previous study suggested that Tgfb3 expression is controlled via upstream cis-regulatory elements in and around the neighboring Ift43 gene. Another study suggested that the canonical Wnt signaling via ß-Catenin is responsible for the MEE-specific Tgfb3 gene expression, since deletion of the Ctnnb1 gene by a commonly used Keratin 14-Cre (K14Cre) mouse line almost completely abolished Tgfb3 expression in the MEE resulting in cleft palate. Here, we wanted to analyze whether Tcf/Lef consensus binding sites located in the previously identified regions of the Ift43 gene are responsible for the spatiotemporal control of Tgfb3 expression during palatogenesis. We show that contrary to the previous report, deletion of the Ctnnb1 gene in basal MEE cells by the K14Cre driver (the same K14Cre mouse line was used as in the previous study referenced above) does not affect the MEE-specific Tgfb3 expression or TGFß3-dependent palatal epithelial fusion. All mutant embryos showed a lack of palatal rugae accompanied by other craniofacial defects, e.g., a narrow snout and a small upper lip, while only a small subset (<5%) of Ctnnb1 mutants displayed a cleft palate. Moreover, the K14Cre:Ctnnb1 embryos showed reduced levels and altered patterns of Shh expression. Our present data imply that epithelial ß-catenin may not be required for MEE-specific Tgfb3 expression or palatal epithelial fusion. |
| first_indexed | 2024-04-09T13:13:18Z |
| format | Article |
| id | doaj.art-4de32e911a1b49d8aecd54bf2ded99ff |
| institution | Directory Open Access Journal |
| issn | 1664-042X |
| language | English |
| last_indexed | 2024-04-09T13:13:18Z |
| publishDate | 2023-05-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Physiology |
| spelling | doaj.art-4de32e911a1b49d8aecd54bf2ded99ff2023-05-12T05:42:43ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2023-05-011410.3389/fphys.2023.704406704406Canonical Wnt signaling is not required for Tgfb3 expression in the basal medial edge epithelium during palatogenesisGhazi-Abdullah Saroya0Erica Siismets1Erica Siismets2Max Hu3Max Hu4Christopher Panaretos5Adam Rice6Kurt Reynolds7Kurt Reynolds8Chengji J. Zhou9Chengji J. Zhou10Vesa Kaartinen11Department of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI, United StatesDepartment of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI, United StatesOral Health Sciences PhD Program, University of Michigan School of Dentistry, Ann Arbor, MI, United StatesDepartment of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI, United StatesCollege of Literature, Sciences and the Arts, University of Michigan, Ann Arbor, MI, United StatesDepartment of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI, United StatesDepartment of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI, United StatesSchool of Medicine, Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children-Northern California, University of California at Davis, Sacramento, CA, United StatesDepartment of Biochemistry and Molecular Medicine, School of Medicine, University of California at Davis, Sacramento, CA, United StatesSchool of Medicine, Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children-Northern California, University of California at Davis, Sacramento, CA, United StatesDepartment of Biochemistry and Molecular Medicine, School of Medicine, University of California at Davis, Sacramento, CA, United StatesDepartment of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI, United StatesThe secondary palate forms from two lateral primordia called the palatal shelves which form a contact in the midline, become adherent at the fusing interface (medial edge epithelia, MEE) and subsequently fuse. The gene encoding transforming growth factor-ß3 (Tgfb3) is strongly and specifically expressed in MEE cells. Our previous study suggested that Tgfb3 expression is controlled via upstream cis-regulatory elements in and around the neighboring Ift43 gene. Another study suggested that the canonical Wnt signaling via ß-Catenin is responsible for the MEE-specific Tgfb3 gene expression, since deletion of the Ctnnb1 gene by a commonly used Keratin 14-Cre (K14Cre) mouse line almost completely abolished Tgfb3 expression in the MEE resulting in cleft palate. Here, we wanted to analyze whether Tcf/Lef consensus binding sites located in the previously identified regions of the Ift43 gene are responsible for the spatiotemporal control of Tgfb3 expression during palatogenesis. We show that contrary to the previous report, deletion of the Ctnnb1 gene in basal MEE cells by the K14Cre driver (the same K14Cre mouse line was used as in the previous study referenced above) does not affect the MEE-specific Tgfb3 expression or TGFß3-dependent palatal epithelial fusion. All mutant embryos showed a lack of palatal rugae accompanied by other craniofacial defects, e.g., a narrow snout and a small upper lip, while only a small subset (<5%) of Ctnnb1 mutants displayed a cleft palate. Moreover, the K14Cre:Ctnnb1 embryos showed reduced levels and altered patterns of Shh expression. Our present data imply that epithelial ß-catenin may not be required for MEE-specific Tgfb3 expression or palatal epithelial fusion.https://www.frontiersin.org/articles/10.3389/fphys.2023.704406/fullbeta-CateninTGF-beta3canonical Wnt signal pathwaypalatogenesiscleft palate (CP) |
| spellingShingle | Ghazi-Abdullah Saroya Erica Siismets Erica Siismets Max Hu Max Hu Christopher Panaretos Adam Rice Kurt Reynolds Kurt Reynolds Chengji J. Zhou Chengji J. Zhou Vesa Kaartinen Canonical Wnt signaling is not required for Tgfb3 expression in the basal medial edge epithelium during palatogenesis Frontiers in Physiology beta-Catenin TGF-beta3 canonical Wnt signal pathway palatogenesis cleft palate (CP) |
| title | Canonical Wnt signaling is not required for Tgfb3 expression in the basal medial edge epithelium during palatogenesis |
| title_full | Canonical Wnt signaling is not required for Tgfb3 expression in the basal medial edge epithelium during palatogenesis |
| title_fullStr | Canonical Wnt signaling is not required for Tgfb3 expression in the basal medial edge epithelium during palatogenesis |
| title_full_unstemmed | Canonical Wnt signaling is not required for Tgfb3 expression in the basal medial edge epithelium during palatogenesis |
| title_short | Canonical Wnt signaling is not required for Tgfb3 expression in the basal medial edge epithelium during palatogenesis |
| title_sort | canonical wnt signaling is not required for tgfb3 expression in the basal medial edge epithelium during palatogenesis |
| topic | beta-Catenin TGF-beta3 canonical Wnt signal pathway palatogenesis cleft palate (CP) |
| url | https://www.frontiersin.org/articles/10.3389/fphys.2023.704406/full |
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