Premium
Temporal regulation of Cre‐recombinase activity in Scl‐positive neurons of the central nervous system
Author(s) -
Bradley Cara K.,
Takano Elena A.,
Göthert Joachim R.,
Göttgens Berthold,
Green Anthony R.,
Begley C. Glenn,
van Eekelen J. Anke M.
Publication year - 2007
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/dvg.20274
Subject(s) - cre recombinase , biology , transgene , genetically modified mouse , enhancer , neurogenesis , central nervous system , gene targeting , hindbrain , cre lox recombination , population , recombinase , microbiology and biotechnology , gene , neuroscience , gene expression , genetics , demography , sociology , recombination
The Cre/LoxP system provides a powerful tool to investigate gene function in vivo. This system requires Cre‐recombinase expressing mouse lines that permit control of gene recombination in a tissue‐specific and time‐dependent manner. To allow spatio‐temporal gene deletion in specific central nervous system (CNS) neuronal populations, we generated mice with a tamoxifen‐inducible Cre (Cre‐ER T ) transgene under control of the Scl/Tal1 neural promoter/enhancer −0.9E3 ( −0.9E3CreER T transgenic mice). Using Cre‐reporter mice we have shown that tamoxifen‐mediated Cre‐ER T recombination in −0.9E3CreER T mice recapitulated the anticipated expression pattern of Scl in the caudal thalamus, midbrain, hindbrain, and spinal cord. Cre‐mediated recombination was also effectively induced during embryogenesis and marked the same population of neurons as observed in the adult. Additionally, we identified a tamoxifen‐independent constitutively active −0.9E3CreER T mouse line that will be useful for gene deletion during early neurogenesis. These −0.9E3CreER T mice will provide tools to investigate the role of neuronal genes in the developing and mature CNS. CNS. genesis 45:145–151, 2007.© 2007 Wiley‐Liss, Inc.