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Floxed allele for conditional inactivation of the voltage‐gated sodium channel β1 subunit Scn1b
Author(s) -
Chen Chunling,
Dickendesher Travis L.,
Oyama Fumitaka,
Miyazaki Haruko,
Nukiobuyuki,
Isom Lori L.
Publication year - 2007
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/dvg.20324
Subject(s) - biology , allele , cre recombinase , genetics , exon , null allele , sodium channel , phenotype , transgene , gene , genetically modified mouse , chemistry , organic chemistry , sodium
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 Scn1b del allele. The null phenotype of Scn1b del 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.