A CamKII alpha iCre BAC allows brain-specific gene inactivation

Citation
E. Casanova et al., A CamKII alpha iCre BAC allows brain-specific gene inactivation, GENESIS, 31(1), 2001, pp. 37-42
Citations number
17
Categorie Soggetti
Cell & Developmental Biology
Journal title
GENESIS
ISSN journal
1526954X → ACNP
Volume
31
Issue
1
Year of publication
2001
Pages
37 - 42
Database
ISI
SICI code
1526-954X(200109)31:1<37:ACAIBA>2.0.ZU;2-K
Abstract
We describe the generation of transgenic mouse lines expressing the Cre rec ombinase enzyme in brain under control of the CamKII alpha. gene present in a BAC expression vector. The CamKII alpha BAC transgene gave a faithful ex pression pattern resembling the pattern of the endogenous CamKII alpha gene . Specifically, high levels of CamKII alpha Cre were detected in hippocampu s, cortex, and amygdala, and lower levels were detected in striatum, thalam us, and hypothalamus. As expected, no expression was detected in the cerebe llum or outside of the brain. The expression level of the BAC CamKII alpha. 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 IoxP sites, and recombination was monitored by the disappear ance of the CREB protein. Finally, evaluation of the developmental postnata l expression of the CamKII alpha Cre BAC revealed the expression of the Cre recombinase as early as P3. (C) 2001 Wiley-Liss, Inc.