ID 109578
Author
Yanuarysuka, Ryna Dwi Department of Molecular Biology, Institute of Health Biosciences, the University of Tokushima Graduate School
Miyoshi, Keiko Department of Molecular Biology, Institute of Health Biosciences, the University of Tokushima Graduate School Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Adiningrat, Arya Department of Molecular Biology, Institute of Health Biosciences, the University of Tokushima Graduate School
Horiguchi, Taigo Department of Molecular Biology, Institute of Health Biosciences, the University of Tokushima Graduate School Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Tanimura, Ayako Department of Molecular Biology, Institute of Health Biosciences, the University of Tokushima Graduate School KAKEN Search Researchers
Hagita, Hiroko Department of Molecular Biology, Institute of Health Biosciences, the University of Tokushima Graduate School
Noma, Takafumi Department of Molecular Biology, Institute of Health Biosciences, the University of Tokushima Graduate School Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Keywords
amelogenesis
dental epithelial cells
Rock1
Sp6
transcription start site
Content Type
Journal Article
Description
Sp6 is a transcription factor of the SP/KLF family and an indispensable regulator
of the morphological dynamics of ameloblast differentiation during tooth development. However, the underlying molecular mechanisms remain unclear. We have previously identified one of the Sp6 downstream genes, Rock1, which is involved in ameloblast polarization. In this study, we investigated the transcriptional regulatory mechanisms of Rock1 by Sp6. First, we identified the transcription start sites (TSS) and cloned the 5'- flanking region of Rock1. Serial deletion analyses identified a critical region for Rock1 promoter activity within the 249-bp upstream region of TSS, and chromatin immunoprecipitation assays revealed Sp6-binding to this region. Subsequent transient transfection experiments showed that Rock1 promoter activity is enhanced by Sp6, but reduced by Sp1. Treatment of dental epithelial cells with the GC-selective DNA binding inhibitor, mithramycin A, affected Rock1 promoter activity in loss of enhancement by Sp6, but not repression by Sp1. Further site-directed mutagenesis indicated that the region from -206 to -150 contains responsive elements for Sp6. Taken together, we conclude that Sp6 positively regulates Rock1 transcription by direct binding to the Rock1 promoter region from -206 to -150, which functionally distinct from Sp1.
Journal Title
The journal of medical investigation : JMI
ISSN
13431420
NCID
AA11166929
Volume
61
Issue
3-4
Start Page
306
End Page
317
Sort Key
306
Published Date
2014-08
EDB ID
FullText File
language
eng
TextVersion
Publisher
departments
Oral Sciences