Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.ydbio.2013.03.008
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dc.titleMurine craniofacial development requires Hdac3-mediated repression of Msx gene expression
dc.contributor.authorSingh, Nikhil
dc.contributor.authorGupta, Mudit
dc.contributor.authorTrivedi, Chinmay M
dc.contributor.authorSingh, Manvendra K
dc.contributor.authorLi, Li
dc.contributor.authorEpstein, Jonathan A
dc.date.accessioned2021-09-28T00:49:17Z
dc.date.available2021-09-28T00:49:17Z
dc.date.issued2013-05-15
dc.identifier.citationSingh, Nikhil, Gupta, Mudit, Trivedi, Chinmay M, Singh, Manvendra K, Li, Li, Epstein, Jonathan A (2013-05-15). Murine craniofacial development requires Hdac3-mediated repression of Msx gene expression. DEVELOPMENTAL BIOLOGY 377 (2) : 333-344. ScholarBank@NUS Repository. https://doi.org/10.1016/j.ydbio.2013.03.008
dc.identifier.issn00121606
dc.identifier.issn1095564X
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/201290
dc.description.abstractCraniofacial development is characterized by reciprocal interactions between neural crest cells and neighboring cell populations of ectodermal, endodermal and mesodermal origin. Various genetic pathways play critical roles in coordinating the development of cranial structures by modulating the growth, survival and differentiation of neural crest cells. However, the regulation of these pathways, particularly at the epigenomic level, remains poorly understood. Using murine genetics, we show that neural crest cells exhibit a requirement for the class I histone deacetylase Hdac3 during craniofacial development. Mice in which Hdac3 has been conditionally deleted in neural crest demonstrate fully penetrant craniofacial abnormalities, including microcephaly, cleft secondary palate and dental hypoplasia. Consistent with these abnormalities, we observe dysregulation of cell cycle genes and increased apoptosis in neural crest structures in mutant embryos. Known regulators of cell cycle progression and apoptosis in neural crest, including Msx1, Msx2 and Bmp4, are upregulated in Hdac3-deficient cranial mesenchyme. These results suggest that Hdac3 serves as a critical regulator of craniofacial morphogenesis, in part by repressing core apoptotic pathways in cranial neural crest cells. © 2013 Elsevier Inc.
dc.language.isoen
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCE
dc.sourceElements
dc.subjectScience & Technology
dc.subjectLife Sciences & Biomedicine
dc.subjectDevelopmental Biology
dc.subjectNeural crest
dc.subjectPalate development
dc.subjectCleft palate
dc.subjectHdac3
dc.subjectMsx1/2
dc.subjectBmp4
dc.subjectNEURAL CREST CELLS
dc.subjectEARLY TOOTH DEVELOPMENT
dc.subjectHISTONE DEACETYLASE 3
dc.subjectCAUSES CLEFT-PALATE
dc.subjectTRANSGENIC MICE
dc.subjectHOMEOBOX GENE
dc.subjectSIGNALING PATHWAYS
dc.subjectSECONDARY PALATE
dc.subjectMORPHOGENESIS
dc.subjectDIFFERENTIATION
dc.typeArticle
dc.date.updated2021-09-22T02:32:14Z
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.1016/j.ydbio.2013.03.008
dc.description.sourcetitleDEVELOPMENTAL BIOLOGY
dc.description.volume377
dc.description.issue2
dc.description.page333-344
dc.published.statePublished
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