Abstract
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 IoxP 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 in vivo inactivation of Scn1b. Conditional inactivation of the 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.
Original language | English |
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Pages (from-to) | 547-553 |
Number of pages | 7 |
Journal | Genesis |
Volume | 45 |
Issue number | 9 |
DOIs | |
Publication status | Published - Sept 2007 |
Externally published | Yes |
Keywords
- β1
- Conditional allele
- Cre/IoxP
- Scn1b
ASJC Scopus subject areas
- Genetics
- Endocrinology
- Cell Biology