SOX7 and SOX17 Regulate the Parietal Endoderm-specific Enhancer Activity of Mouse Laminin α1 Gene

Niimi, Tomoaki; Hayashi, Yoshitaka; Futaki, Sugiko et al.

Journal of Biological Chemistry, 2004, 279(36), 38055-38061

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Identifier to cite or link to this item: https://hdl.handle.net/11094/71429

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Title
SOX7 and SOX17 Regulate the Parietal Endoderm-specific Enhancer Activity of Mouse Laminin α1 Gene
Creator
NRID
1000030377791 1000030377791
CreatorName
Niimi, Tomoaki
NRID
1000080420363 1000080420363
CreatorName
Hayashi, Yoshitaka
NRID
1000000403014 1000000403014
CreatorName
Futaki, Sugiko
NRID
1000050187845 1000050187845
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Scopus Author ID
7201662709 7201662709
ORCID
0000-0002-6433-1410 0000-0002-6433-1410
CreatorName
Sekiguchi, Kiyotoshi
Description
This research was originally published in the Journal of Biological Chemistry. Tomoaki Niimi, Yoshitaka Hayashi, Sugiko Futaki and Kiyotoshi Sekiguchi. SOX7 and SOX17 Regulate the Parietal Endoderm-specific Enhancer Activity of Mouse Laminin α1 Gene. J. Biol. Chem. 2004; 279: 38055-38061 © the American Society for Biochemistry and Molecular Biology
Abstract
Laminin-1 is the major component of embryonic basement membrane and consists of α1, β1, and γ1 chains. The expression of laminin-1 is induced in mouse F9 embryonal carcinoma cells upon differentiation into parietal endoderm cells. We recently identified a parietal endoderm-specific enhancer in the mouse laminin α1 (Lama1) gene and showed that Sp1/Sp3 and YY1 transcription factors were involved in the enhancer activity. Although here we identified that NF-Y binds to the enhancer sequence between Sp1/Sp3- and YY1-binding sites, all these transcription factors are ubiquitously expressed and thus are not sufficient to explain parietal endoderm-specific enhancer activity. In the present study, we further showed that SOX7 and SOX17 are involved in the regulation of parietal endoderm-specific enhancer activity of the mouse Lama1 gene. Northern blot analysis revealed that the steady-state levels of mouse Sox7 and Sox17 mRNAs increased in parallel with that of Lama1 mRNA during the differentiation of F9 cells. Both SOX7 and SOX17 markedly trans-activated the transcription of the Lama1 enhancer-reporter construct in undifferentiated F9 cells in a manner dependent on high mobility group box-mediated DNA binding. Electrophoretic mobility shift assays and mutational analyses revealed that SOX7 and SOX17 bound specifically to two SOX-binding sites within the Lama1 enhancer, and that these SOX-binding sites functioned synergistically to confer the trans-activation by SOX7 and SOX17. Furthermore, this trans-activation was dependent on the integrity of the binding sites for Sp1/Sp3 and NF-Y located at upstream of the two SOX-binding sites. These results indicate that the transcription of the mouse Lama1 gene during the differentiation of F9 cells is controlled by a combination of the actions of the ubiquitous factors, Sp1/Sp3 and NF-Y, and the parietal endoderm-specific factors, SOX7 and SOX17.
Publisher
American Society for Biochemistry and Molecular Biology
Source Title
Journal of Biological Chemistry
Volume (Issue)
279(36)
Page
38055-38061
Date of Issued
2004-09
Language
English
Handle URL
https://hdl.handle.net/11094/71429
eISSN
1083351X
NCID
AA1202441X
Relation.isIdenticalTo
DOI (Publisher Version)
https://doi.org/10.1074/jbc.M403724200
Access Rights
open access
oaire:version
Version of Record
Category
学術雑誌論文 Journal Article