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A CamKIIα iCre BAC allows brain‐specific gene inactivation
Author(s) -
Casanova E.,
Fehsenfeld S.,
Mantamadiotis T.,
Lemberger T.,
Greiner E.,
Stewart A. F.,
Schütz G.
Publication year - 2001
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.1078
Subject(s) - cre recombinase , biology , transgene , genetically modified mouse , microbiology and biotechnology , recombinase , creb , gene expression , gene , genetics , transcription factor , recombination
Summary: We describe the generation of transgenic mouse lines expressing the Cre recombinase enzyme in brain under control of the CamKIIα gene present in a BAC expression vector. The CamKIIα BAC transgene gave a faithful expression pattern resembling the pattern of the endogenous CamKIIα gene. Specifically, high levels of CamKIIα Cre were detected in hippocampus, cortex, and amygdala, and lower levels were detected in striatum, thalamus, and hypothalamus. As expected, no expression was detected in the cerebellum or outside of the brain. The expression level of the BAC CamKIIα driven Cre was shown to be copy number dependent. To test the activity of the Cre recombinase, the transgenic mice were crossed with mice harbouring the CREB (cAMP response element binding protein) allele with the 10th exon flanked by two loxP sites, and recombination was monitored by the disappearance of the CREB protein. Finally, evaluation of the developmental postnatal expression of the CamKIIα Cre BAC revealed the expression of the Cre recombinase as early as P3. genesis 31:37–42, 2001. © 2001 Wiley‐Liss, Inc.