These Kvβ1.1 mutant mice may be useful for neurological studies including hippocampal long-term potentiation, spatial learning, and voltage-gated potassium channels.
Alcino J. Silva, University of California, Los Angeles
Mice homozygous for this Kvβ1.1 targeted allele are viable and fertile. Brain tissue from homozygotes shows no mRNA or protein expression from the targeted allele. Homozygous loss of Kvβ1.1 results in a reduced K+ current inactivation in hippocampal CA1 pyramidal neurons. Homozygous mice have enhanced neuronal excitability that can facilitate long-term potentiation (LTP) induction and improve learning and memory in aged mice (but not in a N7/8 C57BL/6 backcrossed background). Impaired learning in water maze tests and social transmission of food preference tasks is also observed. On a mixed B6;129 genetic background, homozygotes exhibit a prominent reduction in frequency-dependent spike broadening and slow afterhyperpolarization (sAHP) (this phenotype is less prominent on the N7/8 backcrossed C57BL/6 genetic background). These Kvβ1.1 mutant mice may be useful for neurological studies including hippocampal long-term potentiation, spatial learning, and voltage-gated potassium channels.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the donating investigator maintains their colony by breeding heterozygous mice with C57BL/6N. To recapitulate the mixed background for experiments, these mice may be bred with "129 wild-type" mice to generate mutant mice on a "B6;129F1" background. Therefore, the phenotype of these mutant mice congenic (N7/8) on a C57BL/6N genetic background could vary from that originally described. We will modify the strain description if necessary as published results become available.
A targeting vector was designed to insert a PGK-neo cassette into codon 25 of exon 1 of the targeted gene. The construct was electroporated into (129X1/SvJ x 129S1/Sv)F1-derived R1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into blastocysts. The resulting chimeric males were bred with C57BL/6 females, and then intercrossed to generate homozygous Kvβ1.1-deficient mice. These mixed background mice were then backcrossed to C57BL/6NTac for at least seven generations prior to arrival at The Jackson Laboratory. Upon arrival, mutant mice were bred with C57BL/6NJ inbred mice (Stock No. 005304) for at least one generation to establish the colony.
|Allele Name||targeted mutation 1, Alcino J Silva|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Kcnab1, potassium voltage-gated channel, shaker-related subfamily, beta member 1|
|Strain of Origin||(129X1/SvJ x 129S1/Sv)F1-Kitl+|
|Molecular Note||The gene was disrupted by insertion of a PGK-neo cassette into codon 25 of exon 1 via homologous recombination. Northern and Western blot analysis of brain from homozygous mutant animals confirmed the absence of gene expression.|
|Mutations Made By|| |
Alcino Silva, University of California, Los Angeles
When maintaining a live colony, homozygous mice may be bred. The donating investigator maintains their colony by breeding heterozygous mice with C57BL/6N.
When using the B6.129-Kcnab1tm1Sva/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #007747 in your Materials and Methods section.