| First Author | Bradley CK | Year | 2007 |
| Journal | Genesis | Volume | 45 |
| Issue | 3 | Pages | 145-51 |
| PubMed ID | 17330263 | Mgi Jnum | J:121708 |
| Mgi Id | MGI:3711371 | Doi | 10.1002/dvg.20274 |
| Citation | Bradley CK, et al. (2007) Temporal regulation of Cre-recombinase activity in Scl-positive neurons of the central nervous system. Genesis 45(3):145-51 |
| abstractText | 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. |
