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    Neural Crest Deletion of Dlx3 Leads to Major Dentin Defects through Down-regulation of Dspp

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    Authors
    Duverger, Olivier
    Zah, Angela
    Isaac, Juliane
    Sun, Hong-Wei
    Bartels, Anne K.
    Lian, Jane B.
    Berdal, Ariane
    Hwang, Joonsung
    Morasso, Maria I.
    UMass Chan Affiliations
    Department of Cell Biology
    Document Type
    Journal Article
    Publication Date
    2012-04-06
    Keywords
    Transcription Factors
    Homeodomain Proteins
    Dentin
    Neural Crest
    Odontoblasts
    Cell Biology
    
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    Link to Full Text
    http://dx.doi.org/10.1074/jbc.M111.326900
    Abstract
    During development, Dlx3 is expressed in ectodermal appendages such as hair and teeth. Thus far, the evidence that Dlx3 plays a crucial role in tooth development comes from reports showing that autosomal dominant mutations in DLX3 result in severe enamel and dentin defects leading to abscesses and infections. However, the normal function of DLX3 in odontogenesis remains unknown. Here, we use a mouse model to demonstrate that the absence of Dlx3 in the neural crest results in major impairment of odontoblast differentiation and dentin production. Mutant mice develop brittle teeth with hypoplastic dentin and molars with an enlarged pulp chamber and underdeveloped roots. Using this mouse model, we found that dentin sialophosphoprotein (Dspp), a major component of the dentin matrix, is strongly down-regulated in odontoblasts lacking Dlx3. Using ChIP-seq, we further demonstrate the direct binding of Dlx3 to the Dspp promoter in vivo. Luciferase reporter assays determined that Dlx3 positively regulates Dspp expression. This establishes a regulatory pathway where the transcription factor Dlx3 is essential in dentin formation by directly regulating a crucial matrix protein.
    Source
    J Biol Chem. 2012 Apr 6;287(15):12230-40. Epub 2012 Feb 20. Link to article on publisher's site
    DOI
    10.1074/jbc.M111.326900
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/49595
    PubMed ID
    22351765
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1074/jbc.M111.326900
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