Floxed allele for conditional inactivation of the voltage-gated sodium channel β1 subunit Scn1b
Article first published online: 14 SEP 2007
Copyright © 2007 Wiley-Liss, Inc.
Volume 45, Issue 9, pages 547–553, September 2007
How to Cite
Chen, C., Dickendesher, T. L., Oyama, F., Miyazaki, H., Nukina, N. and Isom, L. L. (2007), Floxed allele for conditional inactivation of the voltage-gated sodium channel β1 subunit Scn1b. Genesis, 45: 547–553. doi: 10.1002/dvg.20324
- Issue published online: 14 SEP 2007
- Article first published online: 14 SEP 2007
- Manuscript Accepted: 25 JUN 2007
- Manuscript Received: 1 JUN 2007
- National Multiple Sclerosis Society. Grant Number: RG2882
- NIH. Grant Number: R01 MH059980
- conditional allele;
The voltage-gated sodium channel gene Scn1b encodes the auxiliary subunit β1, which is widely distributed in neurons and glia of the central and peripheral nervous systems, cardiac myocytes, skeletal muscle myocytes, and neuroendocrine cells. We showed previously that the Scn1b null mutation results in a complex and severe phenotype that includes retarded growth, seizures, ataxia, and death by postnatal day 21. We generated a floxed allele of Scn1b by inserting loxP sites surrounding the second coding exon. Ubiquitous deletion of the floxed exon by Cre recombinase using CMV-Cre-transgenic mice produced the Scn1bdel allele. The null phenotype of Scn1bdel homozygotes is indistinguishable from that of Scn1b nulls and confirms the invivo inactivation of Scn1b. Conditional inactivation ofthe floxed allele will make it possible to circumvent the lethality that results from complete loss of this gene, such that the physiological role of Scn1b in specific cell types and/or specific developmental time points can be investigated. genesis 45:547–553, 2007. © 2007 Wiley-Liss, Inc.