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Inducible and neuron‐specific gene expression in the adult mouse brain with the rtTA2S‐M2 system
Author(s) -
Michalon Aubin,
Koshibu Kyoko,
Baumgärtel Karsten,
Spirig Dominique Haingotiana,
Mansuy Isabelle M.
Publication year - 2005
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/gene.20175
Subject(s) - forebrain , transgene , olfactory bulb , reporter gene , biology , gene expression , genetically modified mouse , striatum , transactivation , gene , hippocampus , doxycycline , tyrosine hydroxylase , regulation of gene expression , lac operon , microbiology and biotechnology , neuroscience , genetics , central nervous system , dopamine , antibiotics
Abstract To achieve inducible and reversible gene expression in the adult mouse brain, we exploited an improved version of the tetracycline‐controlled transactivator‐based system (rtTA2 S ‐M2, rtTA2 hereafter) and combined it with the forebrain‐specific CaMKIIα promoter. Several independent lines of transgenic mice carrying the CaMKIIα promoter‐rtTA2 gene were generated and examined for anatomical profile, doxycycline (dox)‐dependence, time course, and reversibility of gene expression using several lacZ reporter lines. In two independent rtTA2‐expressing lines, dox‐treatment in the diet induced lacZ reporter expression in neurons of several forebrain structures including cortex, striatum, hippocampus, amygdala, and olfactory bulb. Gene expression was dose‐dependent and was fully reversible. Further, a similar pattern of expression was obtained in three independent reporter lines, indicating the consistency of gene expression. Transgene expression could also be activated in the developing brain (P0) by dox‐treatment of gestating females. These new rtTA2‐expressing mice allowing inducible and reversible gene expression in the adult or developing forebrain represent useful models for future genetic studies of brain functions. genesis 43:205–212, 2005. © 2005 Wiley‐Liss, Inc.