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Involvement of the Nuclear Factor I Motif in the Mouse Myelin Basic Protein Promoter in Cell‐Specific Regulation: Comparison with the Mouse Glial Fibrillary Acidic Protein Promoter
Author(s) -
Miura Masayuki,
Tamura Takaaki,
Mikoshiba Katsuhiko
Publication year - 1991
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1111/j.1440-169x.1991.00111.x
Subject(s) - microbiology and biotechnology , glial fibrillary acidic protein , promoter , biology , myelin basic protein , transcription (linguistics) , transcription factor , gene expression , gene , myelin , biochemistry , immunohistochemistry , central nervous system , neuroscience , linguistics , philosophy , immunology
We investigated the cis ‐element for cell‐specific expression in the mouse myelin basic protein (MBP) promoter by transfection assay in comparison with that of the glial fibrillary acidic protein (GFAP) promoter. The MBP promoter region including the 1.3 kb upstream region from the transcription start point was found to be highly expressed in NG108–15 cells, a nervous tissue‐derived hybrid cell line, but not in fibroblasts. In contrast, the GFAP promoter region including the region 2.6 kb upstream of the transcription start point was found to function dominantly in C6 glioma cells, but not in NG108–15 cells. Deletion analysis revealed that the NFl motif in the MBP promoter (named MBTE) resulted in the loss of preferential expression in NG108–15 cells. The GFAP promoter also possessed another NFI motif (named GFII) and its distance from the transcription start point was very similar to that of the MBP promoter. Base‐substitution mutation of GFII to MBTE in the GFAP promoter caused remarkable increase in GFAP promoter activity in NG108–15 cells but only slight increase in it activity in C6 cells. These results suggest that the NFI motif in the MBP promoter (MBTE) functions as a cis ‐acting promoter element that governs cell‐specific transcription.