- increased circulating alkaline phosphatase level / IMPC
- decreased thigmotaxis / IMPC
- abnormal epididymis morphology / IMPC
- abnormal behavior / IMPC
- hyperactivity / IMPC
- increased vertical activity / IMPC
- enlarged epididymis / IMPC
- abnormal testis morphology / IMPC
- decreased body length / IMPC
- abnormal auditory brainstem response / IMPC
- limb grasping / IMPC
- preweaning lethality, incomplete penetrance / IMPC
- decreased fasting circulating glucose level / IMPC
B6.129P2-Vti1btm1Gfvm Vti1atm1Gfvm/Ieg
| Status | Available to order |
| EMMA ID | EM:15088 |
| Citation information | RRID:IMSR_EM:15088 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 | B6.129P2-Vti1btm1Gfvm Vti1atm1Gfvm/Ieg |
| Alternative name | vti1a-/- vti1b-/- |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Vti1btm1Gfvm, Vti1atm1Gfvm |
| Gene/Transgene symbol | Vti1b, Vti1a |
Information from provider
| Provider | Gabriele Fischer von Mollard |
| Provider affiliation | Universität Bielefeld |
| Genetic information | A neomycin resistance cassette has been inserted into exon 6 of Vti1a encoding amino acid residues 115-142 by homologous recombination in ES cells. A neomycine resistant cassette has been inserted into exon 4 of Vti1b encoding amino acid residues 123-180 by homologous recombination in ES cells. |
| Phenotypic information | Homozygous:Vti1a-/- Vti1b-/- embryos die perinatally. At E18.5 their frequency is below expectation. They are smaller. Their neuronal development is impaired with defect in major axon tracts, neurodegeneration in several ganglia and malformation in cortical layers.Heterozygous:Vti1a+/- Vti1b+/- are indistinguishable from wild-type and serve as controls in our experiments. |
| Breeding history | The ES cell line E14.1 from 129Ola was used. Offspring was mated with C57BL/6 mice. Mouse strains were maintained with a mixed C57BL/6 x 129/Sv background for several years. Mice were backcrossed to C57BL/6 for 10 generations. Vti1a-/- mice were crossed with Vti1b-/- mice and are now bred as a single strain with Vti1a+/- Vti1b+/-, Vti1a-/- Vti1b+/- and Vti1a+/- Vti1b-/- mice. C57BL/6 is crossed in once or twice a year. |
| References |
|
| Homozygous fertile | no |
| Homozygous viable | no |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | Helmholtz Zentrum Muenchen - German Research Center for Environmental Health (GmbH), Oberschleißheim, Germany |
| Animals used for archiving | heterozygous C57BL/6JRj (Centre D'Elevage R. Janvier) males |
Disease and phenotype information
IMPC phenotypes (gene matching)
Literature references
- Lack of the endosomal SNAREs vti1a and vti1b led to significant impairments in neuronal development.;Kunwar Ajaya J, Rickmann Michael, Backofen Bianca, Browski Sascha M, Rosenbusch Joachim, Schöning Susanne, Fleischmann Thomas, Krieglstein Kerstin, Fischer von Mollard Gabriele, ;2011;Proceedings of the National Academy of Sciences of the United States of America;108;2575-80; 21262811
- Vti1a/b regulate synaptic vesicle and dense core vesicle secretion via protein sorting at the Golgi.;Emperador-Melero Javier, Huson Vincent, van Weering Jan, Bollmann Christian, Fischer von Mollard Gabriele, Toonen Ruud F, Verhage Matthijs, ;2018;Nature communications;9;3421; 30143604
- Primary neurons lacking the SNAREs vti1a and vti1b show altered neuronal development.;Bollmann Christian, Schöning Susanne, Kotschnew Katharina, Grosse Julia, Heitzig Nicole, Fischer von Mollard Gabriele, ;2022;Neural development;17;12; 36419086
- Ablation of Vti1a/1b Triggers Neural Progenitor Pool Depletion and Cortical Layer 5 Malformation in Late-embryonic Mouse Cortex.;Sokpor Godwin, Rosenbusch Joachim, Kunwar Ajaya J, Rickmann Michael, Tuoc Tran, Rizzoli Silvio O, Tarabykin Victor, von Mollard Gabriele Fischer, Krieglstein Kerstin, Staiger Jochen F, ;2021;Neuroscience;463;303-316; 33774122
- Alterations in bone malformation in the absence of the endosomal SNAREs Vti1a and Vti1b.;Schmücker Simone, Schöning Susanne, Wiegand Christiane, Höfling Sascha Michael, Bollmann Christian, Koliwer Judith, Fischer von Mollard Gabriele, ;2026;PloS one;21;e0343070; 41838692
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