B6;129S4-Dlx1tm1(cre/ERT2)Zjh/J

Cat. No.: CEMM-07250293

The Dlx1-CreERT2 knock-in allele was designed to both abolish distal-less homeobox 1 (Dlx1) gene function and direct CreERT2 fusion protein expression to Dlx1 positive neurons (including cortical GABAergic neurons, striatal neurons, and olfactory neurons) by the endogenous Dlx1 promoter/enhancer elements. Cre-ERT2 fusion gene activity is inducible by tamoxifen administration.
Inquiry
Status Live Mouse
Frozen Embryo
Age 4 weeks
12 weeks
Customized Age
Sex Male
Female
GENETICS
Allele Symbol
Dlx1tm1(cre/ERT2)Zjh
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Allele Name
transgene insertion 1
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Allele Attributes
Recombinase-expressing; Inducible
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Gene Symbol
Dlx1
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Gene Name
distal-less homeobox 1
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Chromosome
2
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Expressed Genes
cre/ERT2, Cre recombinase and estrogen receptor 1 (human) fusion gene
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MGI Accession ID show more close
Site of Expression
Following Tamoxifen administration, Cre recombinase activity is observed in Dlx1 positive cortical GABAergic neurons, striatal neurons, and olfactory neurons.
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Strain of Origin
(C57BL/6 x 129S4/SvJae)F1
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Molecular Note
A targeting vector was designed to insert a CreERT2 fusion gene, an SV40 polyA signal, and an FRT flanked neo cassette into the initiation codon of the distal-less homeobox 1 locus (Dlx1). The construct was electroporated into (C57BL/6 x 129S4Sv/Jae)-derived V6.5 embryonic stem (ES) cells. Correctly targeted ES cells were injected into recipient blastocysts and chimeric mice were bred with C57BL/6 mice to originate the colony. The mutation is predicted to result in a null allele. Tamoxifen-inducible Cre recombinase activity recapitulates the endogenous Dlx1 expression pattern, Following tamoxifen administration, Cre recombinase activity is observed in Dlx1 positive cortical GABAergic neurons, striatal neurons, and olfactory neurons.
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HUSBANDRY
Suggested Controls
B6129SF1/J B6129SF2/J
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Breeding Considerations
When maintaining a live colony, heterozygous mice may be bred together, to wildtype siblings, or to C57BL/6J mice. While the donating investigator has not characterized the phenotype of homozygous Dlx1-CreER mice to date, they may be expected to have the same phenotype as other null mutations of this gene (abnormal craniofacial development, cleft palate, and premature death).
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For Research Use Only.
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