B6.129P2-Vti1btm1Gfvm Vti1atm1Gfvm/Ieg

Status

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EMMA IDEM:15088
Citation informationRRID:IMSR_EM:15088 

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International strain nameB6.129P2-Vti1btm1Gfvm Vti1atm1Gfvm/Ieg
Alternative namevti1a-/- vti1b-/-
Strain typeTargeted Mutant Strains : Knock-out
Allele/Transgene symbolVti1btm1Gfvm, Vti1atm1Gfvm
Gene/Transgene symbolVti1b, Vti1a

Information from provider

ProviderGabriele Fischer von Mollard
Provider affiliationUniversität Bielefeld
Genetic informationA 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 informationHomozygous:
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 historyThe 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
  • 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
Homozygous fertileno
Homozygous viableno
Homozygous matings requiredno
Immunocompromisedno

Information from EMMA

Archiving centreHelmholtz Zentrum Muenchen - German Research Center for Environmental Health (GmbH), Oberschleißheim, Germany
Animals used for archivingheterozygous C57BL/6JRj (Centre D'Elevage R. Janvier) males

Disease and phenotype information

IMPC phenotypes (gene matching)
  • 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

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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