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4. Genetic Variants in Protein Tyrosine Phosphatase Non-Receptor Type 23 Are Responsible for Mesiodens Formation

Author

Adisornkanj, Ploy, primary, Chanprasit, Rajit, additional, Eliason, Steven, additional, Fons, Juan M., additional, Intachai, Worrachet, additional, Tongsima, Sissades, additional, Olsen, Bjorn, additional, Arold, Stefan T., additional, Ngamphiw, Chumpol, additional, Amendt, Brad A., additional, Tucker, Abigail S., additional, and Kantaputra, Piranit, additional

Published
2023
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17. Six2 regulates Pax9 expression, palatogenesis and craniofacial bone formation

Author

Sweat, Yan Yan, primary, Sweat, Mason, additional, Mansaray, Maurisa, additional, Cao, Huojun, additional, Eliason, Steven, additional, Adeyemo, Waisu L., additional, Gowans, Lord J.J., additional, Eshete, Mekonen A., additional, Anand, Deepti, additional, Chalkley, Camille, additional, Saadi, Irfan, additional, Lachke, Salil A., additional, Butali, Azeez, additional, and Amendt, Brad A., additional

Published
2020
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21. Missense Pathogenic variants in KIF4A Affect Dental Morphogenesis Resulting in X-linked Taurodontism, Microdontia and Dens-Invaginatus

Author

Gowans, Lord J.J., primary, Cameron-Christie, Sophia, additional, Slayton, Rebecca L., additional, Busch, Tamara, additional, Romero-Bustillos, Miguel, additional, Eliason, Steven, additional, Sweat, Mason, additional, Sobreira, Nara, additional, Yu, Wenjie, additional, Kantaputra, Piranit N., additional, Wohler, Elizabeth, additional, Adeyemo, Wasiu Lanre, additional, Lachke, Salil A., additional, Anand, Deepti, additional, Campbell, Collen, additional, Drummond, Bernadette K., additional, Markie, David M., additional, van Vuuren, W. Jansen, additional, van Vuuren, L. Jansen, additional, Casamassimo, Paul S., additional, Ettinger, Ronald, additional, Owais, Arwa, additional, van Staden, I., additional, Amendt, Brad A., additional, Adeyemo, Adebowale A., additional, Murray, Jeffrey C., additional, Robertson, Stephen P., additional, and Butali, Azeez, additional

Published
2019
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26. FoxO6 regulates Hippo signaling and growth of the craniofacial complex

Author

Sun, Zhao, primary, da Fontoura, Clarissa S. G., additional, Moreno, Myriam, additional, Holton, Nathan E., additional, Sweat, Mason, additional, Sweat, Yan, additional, Lee, Myoung Keun, additional, Arbon, Jed, additional, Bidlack, Felicitas B., additional, Thedens, Daniel R., additional, Nopoulos, Peggy, additional, Cao, Huojun, additional, Eliason, Steven, additional, Weinberg, Seth M., additional, Martin, James F., additional, Moreno-Uribe, Lina, additional, and Amendt, Brad A., additional

Published
2018
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27. Exome Sequencing Provides Additional Evidence for the Involvement of ARHGAP29 in Mendelian Orofacial Clefting and Extends the Phenotypic Spectrum to Isolated Cleft Palate

Author

Liu, Huan, Busch, Tamara, Eliason, Steven, Anand, Deepti, Bullard, Steven, Gowans, Lord J.J, Nidey, Nichole, Petrin, Aline, Augustine-Akpan, Eno-Abasi, Saadi, Irfan, Dunnwald, Martine, Lachke, Salil A., Zhu, Ying, Adeyemo, Adebowale, Amendt, Brad, Roscioli, Tony, Cornell, Robert, Murray, Jeffrey, and Butali, Azeez

Subjects
Male, Cleft Lip, GTPase-Activating Proteins, Computational Biology, High-Throughput Nucleotide Sequencing, Sequence Analysis, DNA, Polymorphism, Single Nucleotide, Article, Pedigree, Cleft Palate, Disease Models, Animal, Gene Frequency, Risk Factors, Exome Sequencing, Animals, Humans, Exome, Female, Alleles, Zebrafish, Genome-Wide Association Study
Abstract

Recent advances in genomics methodologies, in particular the availability of next-generation sequencing approaches have made it possible to identify risk loci throughout the genome, in particular the exome. In the current study, we present findings from an exome study conducted in five affected individuals of a multiplex family with cleft palate only.The GEnome MINIng (GEMINI) pipeline was used to functionally annotate the single nucleotide polymorphisms, insertions and deletions. Filtering methods were applied to identify variants that are clinically relevant and present in affected individuals at minor allele frequencies (≤1%) in the 1000 Genomes Project single nucleotide polymorphism database, Exome Aggregation Consortium, and Exome Variant Server databases. The bioinformatics tool Systems Tool for Craniofacial Expression-Based Gene Discovery was used to prioritize cleft candidates in our list of variants, and Sanger sequencing was used to validate the presence of identified variants in affected and unaffected relatives.Our analyses approach narrowed the candidates down to the novel missense variant in ARHGAP29 (GenBank: NM_004815.3, NP_004806.3;c.1654TC [p.Ser552Pro]. A functional assay in zebrafish embryos showed that the encoded protein lacks the activity possessed by its wild-type counterpart, and migration assays revealed that keratinocytes transfected with wild-type ARHGAP29 migrated faster than counterparts transfected with the p.Ser552Pro ARHGAP29 variant or empty vector (control).These findings reveal ARHGAP29 to be a regulatory protein essential for proper development of the face, identifies an amino acid that is key for this, and provides a potential new diagnostic tool.Birth Defects Research 109:27-37, 2017. © 2016 Wiley Periodicals, Inc.

Published
2017

28. The miR‐200family is required for ectodermal organ development through the regulation of the epithelial stem cell niche

Author

Sweat, Mason, Sweat, Yan, Yu, Wenjie, Su, Dan, Leonard, Riley J., Eliason, Steven L., and Amendt, Brad A.

Abstract

The murine lower incisor ectodermal organ contains a single epithelial stem cell (SC) niche that provides epithelial progenitor cells to the continuously growing rodent incisor. The dental stem cell niche gives rise to several cell types and we demonstrate that the miR‐200family regulates these cell fates. The miR‐200family is highly enriched in the differentiated dental epithelium and absent in the stem cell niche. In this study, we inhibited the miR‐200family in developing murine embryos using new technology, resulting in an expanded epithelial stem cell niche and lack of cell differentiation. Inhibition of individual miRs within the miR‐200cluster resulted in differential developmental and cell morphology defects. miR‐200inhibition increased the expression of dental epithelial stem cell markers, expanded the stem cell niche and decreased progenitor cell differentiation. RNA‐seq. identified miR‐200regulatory pathways involved in cell differentiation and compartmentalization of the stem cell niche. The miR‐200family regulates signaling pathways required for cell differentiation and cell cycle progression. The inhibition of miR‐200decreased the size of the lower incisor due to increased autophagy and cell death. New miR‐200targets demonstrate gene networks and pathways controlling cell differentiation and maintenance of the stem cell niche. This is the first report demonstrating how the miR‐200family is required for in vivo progenitor cell proliferation and differentiation. The LaCL stem cell niche does not express miR‐200, which regulates Sox2 expression. Progenitor cells exiting the stem cell niche start expressing miR‐200 to promote differentiation and the specification of cell fates for mature tooth development. miR‐200 therefore acts to compartmentalize the stem cell niche

Published
2021
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38. Exome sequencing provides additional evidence for the involvement of ARHGAP29 in Mendelian orofacial clefting and extends the phenotypic spectrum to isolated cleft palate

Author

Liu, Huan, primary, Busch, Tamara, additional, Eliason, Steven, additional, Anand, Deepti, additional, Bullard, Steven, additional, Gowans, Lord J.J, additional, Nidey, Nichole, additional, Petrin, Aline, additional, Augustine‐Akpan, Eno‐Abasi, additional, Saadi, Irfan, additional, Dunnwald, Martine, additional, Lachke, Salil A., additional, Zhu, Ying, additional, Adeyemo, Adebowale, additional, Amendt, Brad, additional, Roscioli, Tony, additional, Cornell, Robert, additional, Murray, Jeffrey, additional, and Butali, Azeez, additional

Published
2017
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42. Sox2 and Lef-1 interact with Pitx2 to regulate incisor development and stem cell renewal

Author

Sun, Zhao, primary, Yu, Wenjie, additional, Navarro, Maria Sanz, additional, Sweat, Mason, additional, Eliason, Steven, additional, Sharp, Thad, additional, Liu, Huan, additional, Seidel, Kerstin, additional, Zhang, Li, additional, Moreno, Myriam, additional, Lynch, Thomas, additional, Holton, Nathan E., additional, Rogers, Laura, additional, Neff, Traci, additional, Goodheart, Michael J., additional, Michon, Frederic, additional, Klein, Ophir D., additional, Chai, Yang, additional, Dupuy, Adam, additional, Engelhardt, John F., additional, Chen, Zhi, additional, and Amendt, Brad A., additional

Published
2016
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44. Sox2 and Lef-1 interact with Pitx2 to regulate incisor development and stem cell renewal.

Author

Zhao Sun, Wenjie Yu, Sweat, Mason, Eliason, Steven, Sharp, Thad, Moreno, Myriam, Lynch, Thomas, Rogers, Laura, Neff, Traci, Dupuy, Adam, Engelhardt, John F., Huan Liu, Amendt, Brad A., Navarro, Maria Sanz, Michon, Frederic, Li Zhang, Zhi Chen, Seidel, Kerstin, Klein, Ophir D., and Holton, Nathan E.

Subjects
STEM cells, CLEFT palate, INCISORS
Abstract

Sox2 marks dental epithelial stem cells (DESCs) in both mammals and reptiles, and in this article we demonstrate several Sox2 transcriptional mechanisms that regulate dental stem cell fate and incisor growth. Conditional Sox2 deletion in the oral and dental epithelium results in severe craniofacial defects, including impaired dental stem cell proliferation, arrested incisor development and abnormal molar development. The murine incisor develops initially but is absorbed independently of apoptosis owing to a lack of progenitor cell proliferation and differentiation. Tamoxifen-induced inactivation of Sox2 demonstrates the requirement of Sox2 for maintenance of the DESCs in adult mice. Conditional overexpression of Lef-1 in mice increases DESC proliferation and creates a new labial cervical loop stem cell compartment, which produces rapidly growing long tusk-like incisors, and Lef-1 epithelial overexpression partially rescues the tooth arrest in Sox2 conditional knockout mice. Mechanistically, Pitx2 and Sox2 interact physically and regulate Lef-1, Pitx2 and Sox2 expression during development. Thus, we have uncovered a Pitx2-Sox2-Lef-1 transcriptional mechanism that regulates DESC homeostasis and dental development. [ABSTRACT FROM AUTHOR]

Published
2016
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48. TBX1 protein interactions and microRNA-96-5p regulation controls cell proliferation during craniofacial and dental development: implications for 22q11.2 deletion syndrome

Author

Henry C. Margolis, Myriam Moreno, Wenjie Yu, Huojun Cao, Shan Gao, Felicitas B. Bidlack, Xiao Li, Antonio Baldini, Brad A. Amendt, Steven Eliason, Gao, Shan, Moreno, Myriam, Eliason, Steven, Cao, Huojun, Li, Xiao, Yu, Wenjie, Bidlack, Felicitas B, Margolis, Henry C, Baldini, Antonio, and Amendt, Brad A.

Subjects
TBX1, Male, Biology, Facial Bones, Craniofacial Abnormalities, Mice, stomatognathic system, DiGeorge syndrome, Conditional gene knockout, Genetics, medicine, DiGeorge Syndrome, Animals, Humans, Craniofacial, Progenitor cell, Promoter Regions, Genetic, Molecular Biology, Genetics (clinical), Cell Proliferation, Regulation of gene expression, PITX2, Gene Expression Regulation, Developmental, General Medicine, Articles, medicine.disease, Cell biology, stomatognathic diseases, MicroRNAs, embryonic structures, Female, Stem cell, T-Box Domain Proteins, Tooth, Protein Binding
Abstract

T-box transcription factor TBX1 is the major candidate gene for 22q11.2 deletion syndrome (22q11.2DS, DiGeorge syndrome/Velo-cardio-facial syndrome), whose phenotypes include craniofacial malformations such as dental defects and cleft palate. In this study, Tbx1 was conditionally deleted or over-expressed in the oral and dental epithelium to establish its role in odontogenesis and craniofacial developmental. Tbx1 lineage tracing experiments demonstrated a specific region of Tbx1-positive cells in the labial cervical loop (LaCL, stem cell niche). We found that Tbx1 conditional knockout (Tbx1(cKO)) mice featured microdontia, which coincides with decreased stem cell proliferation in the LaCL of Tbx1(cKO) mice. In contrast, Tbx1 over-expression increased dental epithelial progenitor cells in the LaCL. Furthermore, microRNA-96 (miR-96) repressed Tbx1 expression and Tbx1 repressed miR-96 expression, suggesting that miR-96 and Tbx1 work in a regulatory loop to maintain the correct levels of Tbx1. Cleft palate was observed in both conditional knockout and over-expression mice, consistent with the craniofacial/tooth defects associated with TBX1 deletion and the gene duplication that leads to 22q11.2DS. The biochemical analyses of TBX1 human mutations demonstrate functional differences in their transcriptional regulation of miR-96 and co-regulation of PITX2 activity. TBX1 interacts with PITX2 to negatively regulate PITX2 transcriptional activity and the TBX1 N-terminus is required for its repressive activity. Overall, our results indicate that Tbx1 regulates the proliferation of dental progenitor cells and craniofacial development through miR-96-5p and PITX2. Together, these data suggest a new molecular mechanism controlling pathogenesis of dental anomalies in human 22q11.2DS.

Published
2015

49. miR-17 acts as a tumor suppressor by negatively regulating the miR-17-92 cluster.

Author

Sweat Y, Ries RJ, Sweat M, Su D, Shao F, Eliason S, and Amendt BA

Abstract

Anaplastic thyroid cancer (ATC) is an aggressive, highly metastatic cancer that expresses high levels of the microRNA ( miR)-17-92 cluster. We employ an miR inhibitor system to study the function of the different miRs within the miR-17-92 cluster based on seed sequence homology in the ATC SW579 cell line. While three of the four miR-17-92 families were oncogenic, we uncovered a novel role for miR-17 as a tumor suppressor in vitro and in vivo . Surprisingly, miR-17 inhibition increased expression of the miR-17-92 cluster and significantly increased the levels of the miR-18a and miR-19a mature miRs. miR-17 inhibition increased expression of the cell cycle activator CCND2, associated with increased cell proliferation and tumor growth in transplanted SW579 cells in xenograft mice. miR-17 regulates MYCN and c-MYC expression in SW579 cells, and the inhibition of miR-17 increased MYCN and c-MYC expression, which increased pri-miR-17-92 transcripts. Thus, inhibition of miR-17 activated the expression of the oncogenic miRs, miR-18a and miR-19a . While many cancers express high levels of miR-17 , linking it with tumorigenesis, we demonstrate that miR-17 inhibition does not inhibit thyroid tumor growth in SW579 and MDA-T32 ATC cells but increases expression of the other miR-17-92 family members and genes to induce cancer progression., Competing Interests: B.A.A. is the owner and Chief Scientific Officer of NaturemiRI, and PMIS microRNA inhibitors., (© 2021 The Author(s).)

Published
2021
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50. Pitx2-Sox2-Lef1 interactions specify progenitor oral/dental epithelial cell signaling centers.

Author

Yu W, Sun Z, Sweat Y, Sweat M, Venugopalan SR, Eliason S, Cao H, Paine ML, and Amendt BA

Subjects
Adaptor Proteins, Signal Transducing genetics, Adaptor Proteins, Signal Transducing metabolism, Animals, Cell Cycle Proteins genetics, Cell Cycle Proteins metabolism, Cell Differentiation, Cell Proliferation, Dental Enamel metabolism, Embryo, Mammalian metabolism, Epithelial Cells cytology, Gene Expression Regulation, Developmental, Hedgehog Proteins metabolism, Homeodomain Proteins genetics, Lymphoid Enhancer-Binding Factor 1 genetics, Mice, Mice, Knockout, Odontogenesis, SOXB1 Transcription Factors genetics, Stem Cell Niche, Stem Cells cytology, Stem Cells metabolism, Tooth cytology, Tooth growth & development, Tooth metabolism, Transcription Factors deficiency, Transcription Factors genetics, YAP-Signaling Proteins, Homeobox Protein PITX2, Epithelial Cells metabolism, Homeodomain Proteins metabolism, Lymphoid Enhancer-Binding Factor 1 metabolism, SOXB1 Transcription Factors metabolism, Signal Transduction, Transcription Factors metabolism
Abstract

Epithelial signaling centers control epithelial invagination and organ development, but how these centers are specified remains unclear. We report that Pitx2 (the first transcriptional marker for tooth development) controls the embryonic formation and patterning of epithelial signaling centers during incisor development. We demonstrate using Krt14 Cre / Pitx2 flox/flox ( Pitx2 cKO ) and Rosa26 CreERT /Pitx2 flox/flox mice that loss of Pitx2 delays epithelial invagination, and decreases progenitor cell proliferation and dental epithelium cell differentiation. Developmentally, Pitx2 regulates formation of the Sox2 + labial cervical loop (LaCL) stem cell niche in concert with two signaling centers: the initiation knot and enamel knot. The loss of Pitx2 disrupted the patterning of these two signaling centers, resulting in tooth arrest at E14.5. Mechanistically, Pitx2 transcriptional activity and DNA binding is inhibited by Sox2, and this interaction controls gene expression in specific Sox2 and Pitx2 co-expression progenitor cell domains. We demonstrate new transcriptional mechanisms regulating signaling centers by Pitx2 , Sox2 , Lef1 and Irx1 ., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2020. Published by The Company of Biologists Ltd.)

Published
2020
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