129S4(B6N)-Slc1a3tm1.1(cre/ERT2)Wsj/WsjH
Status | Available to order |
EMMA ID | EM:11807 |
International strain name | 129S4(B6N)-Slc1a3tm1.1(cre/ERT2)Wsj/WsjH |
Alternative name | Slc1a3-CreERT2 |
Strain type | Targeted Mutant Strains : Knock-in |
Allele/Transgene symbol | Slc1a3tm1.1(cre/ERT2)Wsj |
Gene/Transgene symbol | Slc1a3 |
Information from provider
Provider | Walker Jackson |
Provider affiliation | Clinical and Experimental Medicine, Linköping University |
Genetic information | Sequence encoding the Cre-ERT2 fusion protein was inserted in place of the stop codon of the sequence encoding Slc1a3. A 2A peptide separates the two proteins during translation. |
Phenotypic information | Homozygous:This line expresses Cre-ERT2 from the Slc1a3 (or GLAST) locus, leaving the native protein coding sequence intact. The mice appear normal as homozygotes. The oldest age observed is 6 months. The line is still new so not fully characterized. Homozygotes are easily distinguished from heterozygotes by the standard PCR assay.Heterozygous:Heterozygotes appear no different from homozygotes or wild-type mice |
Breeding history | The allele was targeted into J1 129S4 ES cells. Chimeras were bred to mice expressing Flp recombinase (from the ROSA26 locus) to remove the selectable marker (neo) that was inserted approximately 200 base pairs downstream of the stop codon. The Flp mice were obtained from Jax on a 129S4 background and were bred in house to carry wild-type Disc1 and the non-agouti gene from C57BL/6N mice. The final genetic background of the Flp mice is >99% 129S4, verified by SNP analysis. The F1 and F2 generations were bred to 129S4 to reintroduce natural alleles of Disc1, agouti, and ROSA26 from 129S4. F3 and F4 generations were intercrossed to generate and expand a homozygous line. They currently exist at the F5 generation. |
References |
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Homozygous fertile | yes |
Homozygous viable | yes |
Homozygous matings required | no |
Immunocompromised | no |
Information from EMMA
Archiving centre | Mary Lyon Centre at MRC Harwell, Oxford, United Kingdom |
Disease and phenotype information
Orphanet associated rare diseases, based on orthologous gene matching
- Episodic ataxia type 6 / Orphanet_209967
IMPC phenotypes (gene matching)
MGI phenotypes (gene matching)
- abnormal Purkinje cell morphology / MGI
- retinal degeneration / MGI
- abnormal optic nerve morphology / MGI
- abnormal kindling response / MGI
- abnormal motor coordination/balance / MGI
- seizures / MGI
- increased susceptibility to pharmacologically induced seizures / MGI
- abnormal excitatory postsynaptic currents / MGI
- increased lactate dehydrogenase level / MGI
- nervous system phenotype / MGI
- abnormal nervous system physiology / MGI
- abnormal retinal inner nuclear layer morphology / MGI
- cochlear inner hair cell degeneration / MGI
- abnormal synaptic glutamate release / MGI
- increased susceptibility to noise-induced hearing loss / MGI
- increased susceptibility to ototoxicity-induced hearing loss / MGI
- abnormal retinal ganglion layer morphology / MGI
- behavior/neurological phenotype / MGI
- vision/eye phenotype / MGI
- optic nerve cupping / MGI
- optic nerve degeneration / MGI
- decreased retinal ganglion cell number / MGI
- increased cellular sensitivity to hydrogen peroxide / MGI
- abnormal auditory brainstem response waveform shape / MGI
- increased or absent threshold for auditory brainstem response / MGI
- abnormal electroretinogram waveform feature / MGI
Literature references
- Slc1a3-2A-CreERT2 mice reveal unique features of Bergmann glia and augment a growing collection of Cre drivers and effectors in the 129S4 genetic background.;Kaczmarczyk Lech, Reichenbach Nicole, Blank Nelli, Jonson Maria, Dittrich Lars, Petzold Gabor C, Jackson Walker S, ;2021;Scientific reports;11;5412; 33686166
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