STOCK Hdac2^tm1.2Rdp/J

Stock number: 012640
Research areas: Neurobiology Research

Description

These HDAC2KO mutant mice lack exons 5-6 of the mouse histone deacetylase 2 (Hdac2) gene. This strain may be useful for studying the functional and structural synaptic changes and neuronal adaptive responses implicated in memory formation and storage.

Detailed description

These HDAC2KO mutant mice lack exons 5-6 of the mouse histone deacetylase 2 (Hdac2) gene. Mice that are homozygous for this allele are viable, with reduced fertility, and are born at a twofold lower frequency than expected from a normal Mendelian ratio. Homozygous mutants are about 25% smaller than wild-type and heterozygote littermates. These mice have an increased synapse number and enhanced memory formation. This strain may be useful for studying the functional and structural synaptic changes and neuronal adaptive responses implicated in memory formation and storage.

Development

A targeting vector was designed to insert a loxP site upstream of exon 5 and a loxP site downstream of exon 6 of the mouse histone deacetylase 2 (Hdac2) gene. The construct was electroporated into embryonic stem (ES) cells, and correctly targeted ES cells were injected into blastocysts. The resulting chimeric mice were bred to FVB/N to generate a colony of Hdac2^L mice. These floxed mice were then bred to mice carrying cre recombinase on a C57BL/6 background to remove the floxed exons. These HDAC2KO mice were maintained on an FVB X C57BL/6 background. Upon arrival at The Jackson Laboratory, mice were bred to C57BL/6J inbred mice (Stock No. 000664) for at least one generation to establish the colony.

Allele

Symbol: Hdac2^tm1.2Rdp
Name: targeted mutation 1.2, Ronald DePinho
MGI accession ID: MGI:3844984
Generation method: Targeted
Attributes: Null/Knockout
Marker symbol: Hdac2
Marker name: histone deacetylase 2
Chromosome: 10
Strain of origin: (C57BL/6 x 129S4/SvJae)F1
Molecular note: LoxP sites were inserted upstream of exon 5 and downstream of exon 6. Mice carrying this allele were crossed with mice expressing cre recombinase in the germline. Gene inactivation was confirmed by a lack of signal in immunoblot analysis of homozygote brain extracts. The same analysis showed that expression of related Hdac1 protein was upregulated.