These Rims1 knock-out mice exhibit decreased transmitter release at inhibitory synapses and an increase at excitatory synapses. They may be useful in studies relating to neurotransmission.
Dr. Thomas C. Sudhof, Stanford University School of Medicine
Genetic Background | Generation |
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|
Allele Type | Gene Symbol | Gene Name |
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Targeted (Null/Knockout) | Rims1 | regulating synaptic membrane exocytosis 1 |
Mice homozygous for this targeted mutation are viable and fertile, but are poor breeders. Morphological analyses of the brain failed to uncover structural abnormalities or changes in brain architecture. Protein product from the targeted gene is not detected in brain tissue. No statistically significant difference in the density and size of synapses, synaptic vesicle density, or number of docked vesicles has been detected. Decreased transmitter release during paired stimulations was found at inhibitory synapses, opposite to an increase at excitatory synapses. Post-tetanic potentiation (short-term plasticity) is strongly enhanced. This mutant mouse strain represents a model that may be useful in studies of neurotransmitter release.
Targeting vectors containing a neomycin resistance gene were used to replace the first coding exon of the targeted gene. The constructs were electroporated into 129P2/OlaHsd-derived E14.1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. Chimeric animals were crossed with C57BL/6 for at least three generations.
Allele Name | targeted mutation 1, Thomas C Sudhof |
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Allele Type | Targeted (Null/Knockout) |
Allele Synonym(s) | RIM1alpha-; Rim1alphamt |
Gene Symbol and Name | Rims1, regulating synaptic membrane exocytosis 1 |
Gene Synonym(s) | |
Strain of Origin | 129P2/OlaHsd |
Chromosome | 1 |
Molecular Note | A neomycin resistance cassette replaced the first coding exon, which encodes the translation initiation site and 55 conserved N-terminal residues. Immunoblot analysis using antibody to the N-terminal zinc finger domain did not detect protein. |
Mutations Made By | Dr. Thomas Sudhof, Stanford University School of Medicine |
When maintained as a live colony, heterozygotes are intercrossed. Homozygotes are both viable and fertile, but the males are inefficient breeders and the females are poor mothers
When using the RIM1α KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #006376 in your Materials and Methods section.
Facility Barrier Level Descriptions
Service/Product | Description | Price |
---|---|---|
Heterozygous or Wild-type for Rims1<tm1Sud> |
Frozen Mouse Embryo | B6;129P2-Rims1<tm1Sud>/J Frozen Embryo | $2595.00 |
Frozen Mouse Embryo | B6;129P2-Rims1<tm1Sud>/J Frozen Embryo | $2595.00 |
Frozen Mouse Embryo | B6;129P2-Rims1<tm1Sud>/J Frozen Embryo | $3373.50 |
Frozen Mouse Embryo | B6;129P2-Rims1<tm1Sud>/J Frozen Embryo | $3373.50 |
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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.
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