- decreased insulin secretion / MGI
- abnormal pancreatic islet morphology / MGI
- impaired glucose tolerance / MGI
- weakness / MGI
- abnormal CNS synaptic transmission / MGI
- nervous system phenotype / MGI
- decreased neurotransmitter release / MGI
- abnormal synaptic vesicle number / MGI
- decreased pulmonary respiratory rate / MGI
- absent gastric milk in neonates / MGI
- postnatal lethality, complete penetrance / MGI
- neonatal lethality, complete penetrance / MGI
B6.129-Unc13atm1Bros/Ph
| Status | Available to order |
| EMMA ID | EM:11244 |
| Citation information | RRID:IMSR_EM:11244 Research Resource Identifiers (RRID) are persistent unique ID numbers assigned to help researchers cite key resources (e.g. antibodies, model organisms and software projects) in the biomedical literature to improve transparency and reproducibility in research. See https://www.rrids.org/ for more information. |
| International strain name | B6.129-Unc13atm1Bros/Ph |
| Alternative name | Unc13a tm1Bros |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Unc13atm1Bros |
| Gene/Transgene symbol | Unc13a |
Information from provider
| Provider | Nils Brose |
| Provider affiliation | Department of Molecular Neurobiology, Max Planck Institute of Experimental Medicine |
| Genetic information | In the targeting vector, four exons, representing base pairs 2587 to 2964 of rat Munc13-1, were replaced with a neomycin resistance gene. Upon homologous recombination of the targeting vector with the Munc13-1 gene, the insertion of the neomycin resistance cassette results in the deletion of amino-acid residues 494 to 618 (including the C1 domain) and a shift in the open reading frame of the mature messenger RNA. |
| Phenotypic information | Homozygous:Munc13-1-deficient mice do not feed and are distinguishable from wild-type animals shortly after birth by a lack of milk in their stomachs, weakness and reduced breathing rate. Mutant mice die within a few hours of birth.Heterozygous:Heterozygous mice are normal and show no obvious alterations in comparison to wild-type controls. |
| Breeding history | Homologous recombination in 129/Sv embryonic stem cells, consecutive backcrosses with C57BL/6J animals. |
| References |
|
| Homozygous fertile | no |
| Homozygous viable | no |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | Institute of Molecular Genetics, Prague, Czech Republic |
| Animals used for archiving | heterozygous C57BL/6 x 129/Sv males |
Disease and phenotype information
MGI phenotypes (allele matching)
MGI phenotypes (gene matching)
- weakness / MGI
- abnormal CNS synaptic transmission / MGI
- abnormal excitatory postsynaptic currents / MGI
- decreased synaptic depression / MGI
- decreased insulin secretion / MGI
- nervous system phenotype / MGI
- decreased neurotransmitter release / MGI
- abnormal synaptic vesicle morphology / MGI
- abnormal synaptic vesicle recycling / MGI
- abnormal synaptic vesicle number / MGI
- abnormal neuron physiology / MGI
- abnormal pancreatic islet morphology / MGI
- impaired glucose tolerance / MGI
- homeostasis/metabolism phenotype / MGI
- reproductive system phenotype / MGI
- decreased pulmonary respiratory rate / MGI
- absent gastric milk in neonates / MGI
- postnatal lethality, complete penetrance / MGI
- neonatal lethality, complete penetrance / MGI
Literature references
- Munc13-1 is essential for fusion competence of glutamatergic synaptic vesicles.;Augustin I, Rosenmund C, Südhof T C, Brose N, ;1999;Nature;400;457-61; 10440375
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