C.129S4(B6)-Gsntm1Djk/Cnrm

Status

Available to order

EMMA IDEM:09464
International strain nameC.129S4(B6)-Gsntm1Djk/Cnrm
Alternative nameBalbC GSN KO
Strain typeTargeted Mutant Strains : Knock-out
Allele/Transgene symbolGsntm1Djk
Gene/Transgene symbolGsn

Information from provider

ProviderWalter Witke
Provider affiliationInstitute of Genetics, University Bonn
Genetic informationGelsolin KO mutation crossed with mice of BALB/c inbred background.
Phenotypic informationHomozygous:
In the context of a BALB/c background, the Gsn(-/-) mutation causes embryonic death. A significant first reduction of null mutant embryos was observed by day 13.5. Few homozygous mutant embryos were present by 17.5-18.5 days of gestation and increased presence of resorbed embryos. Moreover, Gsn(-/-) embryos show defective erythroid maturation with persistence of circulating nucleated cells.

Heterozygous:
Heterozygous mice in a BALB/c background developed normally, were fertile and showed no obvious abnormalities.
Breeding historyMice with a C57BL/6 outbred background homozygous for the mutation were crossed with mice of BALB/c inbred background. Among the F1 animals, mice heterozygous for the mutation were selected by genotyping. These F1 animals were crossed with mice of BALB/c inbred background to produce F2 progeny, among which only mice heterozygous for the mutation were used for the next generation. The same cycle was repeated until F10 mice were obtained. Heterozygous F10 mice were crossed to produce mice homozygous for the mutation, with a genetic background very close to the BALB/c inbred background.
References
  • Defective erythroid maturation in gelsolin mutant mice.;Cantù Claudio, Bosè Francesca, Bianchi Paola, Reali Eva, Colzani Maria Teresa, Cantù Ileana, Barbarani Gloria, Ottolenghi Sergio, Witke Walter, Spinardi Laura, Ronchi Antonella Ellena, ;2012;Haematologica;97;980-8; 22271892
Homozygous fertileno
Homozygous viableno
Homozygous matings requiredno
Immunocompromisedno

Information from EMMA

Archiving centreCNR, Consiglio Nazionale delle Ricerche, Monterotondo, Italy

Disease and phenotype information

Orphanet associated rare diseases, based on orthologous gene matching

MGI phenotypes (allele matching)
  • abnormal branching of the mammary ductal tree / MGI
  • abnormal mammary gland growth during pregnancy / MGI
  • lethality throughout fetal growth and development, complete penetrance / MGI
  • abnormal mammary duct terminal end bud morphology / MGI
  • osteopetrosis / MGI
  • increased leukocyte cell number / MGI
  • increased neutrophil cell number / MGI
  • abnormal skeleton physiology / MGI
  • abnormal osteoclast physiology / MGI
  • abnormal immune system physiology / MGI
  • decreased inflammatory response / MGI
  • premature death / MGI
  • abnormal bone remodeling / MGI
  • abnormal long bone epiphyseal plate morphology / MGI
  • increased compact bone thickness / MGI
  • abnormal long bone diaphysis morphology / MGI
  • abnormal wound healing / MGI
  • abnormal platelet physiology / MGI
  • abnormal skeleton morphology / MGI
  • increased bleeding time / MGI
  • abnormal osteoclast differentiation / MGI
  • impaired neutrophil recruitment / MGI
  • impaired neutrophil chemotaxis / MGI
  • abnormal nervous system electrophysiology / MGI
  • abnormal pulmonary circulation / MGI
  • increased vascular permeability / MGI
  • increased susceptibility to ischemic brain injury / MGI
  • increased cerebral infarction size / MGI
MGI phenotypes (gene matching)
  • osteopetrosis / MGI
  • increased leukocyte cell number / MGI
  • increased neutrophil cell number / MGI
  • abnormal branching of the mammary ductal tree / MGI
  • abnormal skeleton physiology / MGI
  • abnormal osteoclast physiology / MGI
  • abnormal immune system physiology / MGI
  • decreased inflammatory response / MGI
  • premature death / MGI
  • abnormal nervous system electrophysiology / MGI
  • abnormal pulmonary circulation / MGI
  • abnormal bone remodeling / MGI
  • abnormal long bone epiphyseal plate morphology / MGI
  • increased vascular permeability / MGI
  • increased susceptibility to ischemic brain injury / MGI
  • increased compact bone thickness / MGI
  • abnormal long bone diaphysis morphology / MGI
  • abnormal wound healing / MGI
  • abnormal platelet physiology / MGI
  • abnormal skeleton morphology / MGI
  • increased bleeding time / MGI
  • increased cerebral infarction size / MGI
  • abnormal mammary gland growth during pregnancy / MGI
  • abnormal osteoclast differentiation / MGI
  • impaired neutrophil recruitment / MGI
  • impaired neutrophil chemotaxis / MGI
  • lethality throughout fetal growth and development, complete penetrance / MGI
  • abnormal mammary duct terminal end bud morphology / MGI

Literature references

  • Defective erythroid maturation in gelsolin mutant mice.;Cantù Claudio, Bosè Francesca, Bianchi Paola, Reali Eva, Colzani Maria Teresa, Cantù Ileana, Barbarani Gloria, Ottolenghi Sergio, Witke Walter, Spinardi Laura, Ronchi Antonella Ellena, ;2012;Haematologica;97;980-8; 22271892

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Availabilities

Requesting frozen sperm or embryos is generally advisable wherever possible, in order to minimise the shipment of live mice.

  • Frozen embryos. Delivered in 4 weeks (after paperwork in place). €1740*
  • Frozen sperm. Delivered in 4 weeks (after paperwork in place). €1740*
  • Rederivation of mice from frozen stock, delivery time available upon request . €3880*

Due to the dynamic nature of our processes strain availability may change at short notice. The local repository manager will advise you in these circumstances.

* In addition users have to cover all the shipping costs (including the cost for returning dry-shippers, where applicable).

More details on pricing and delivery times

Practical information

Example health report
(Current health report will be provided later)

Material Transfer Agreement (MTA)
For this strain no provider MTA is needed. Distribution is based on the EMMA conditions only.

EMMA conditions
Legally binding conditions for the transfer

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