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Normal and pathological expression of GFAP promoter elements in transgenic mice
Author(s) -
Galou M.,
Pournin S.,
Ensergueix D.,
Ridet J.L.,
Tchélingérian J.L.,
Lossouran L.,
Privat A.,
Babinet C.,
Dupouey P.
Publication year - 1994
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.440120405
Subject(s) - transgene , biology , glial fibrillary acidic protein , genetically modified mouse , astrocyte , gliosis , microbiology and biotechnology , reporter gene , gene , vimentin , regulatory sequence , gene expression , genetics , central nervous system , immunohistochemistry , immunology , neuroscience
The expression of the glial fibrillary acidic protein (GFAP), a component of astroglial intermediate filaments, is regulated under developmental and pathological conditions. In order to characterize DNA sequences involved in such regulations, we produced transgenic mice bearing 2 kb of the 5′ flanking region of the murine GFAP gene linked to the Escherichia coli β‐galactosidase (β‐gal) reporter gene. Seven transgenic lines were obtained. We observed that the regulatory elements present in the transgene GFAP‐nls‐LacZ direct an expression in the neural and non‐neural tissue and target in vivo an unexpected subpopulation of astrocyte. In the developing brain, β‐gal activity and GFAP appeared simultaneously and in the same region, on embryonic day 18 (E18), suggesting that the 2 kb of the promoter contains the regulatory sequences responsible for the perinatal vimentin/GFAP switch. In addition, we demonstrated that the 2 kb sequence of the GFAP promoter used in the transgene possess elements which are activated after a surgical injury, thus permitting to study some aspects of reactive gliosis in these transgenic mice. These transgenic lines provide a useful tool by enabling further studies of astroglial and, probably, neuronal physilogies.