- decreased body weight / MGI
- abnormal placenta labyrinth morphology / MGI
- postnatal growth retardation / MGI
- no phenotypic analysis / MGI
- fetal growth retardation / MGI
- abnormal placental labyrinth vasculature morphology / MGI
- decreased fetal weight / MGI
- preweaning lethality, incomplete penetrance / MGI
- abnormal syncytiotrophoblast morphology / MGI
CBA.129S2(B6)-Synbtm2.1Ics/Orl
Status | Available to order |
EMMA ID | EM:11297 |
Citation information | RRID:IMSR_EM:11297 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 | CBA.129S2(B6)-Synbtm2.1Ics/Orl |
Alternative name | CBA/J Syncytin-B KI |
Strain type | Targeted Mutant Strains : Knock-in |
Allele/Transgene symbol | Synbtm2.1Ics |
Gene/Transgene symbol | Synb |
Information from provider
Provider | Thierry Heidmann |
Provider affiliation | Insitut Gustave Roussy, UMR9196 CNRS |
Genetic information | Mice carrying a mutated copy of the syncytin-B gene (point mutation in the immunosuppressive ISU domain), that abolishes its immunosuppressive activity without altering its fusogenic properties. This strain was obtained via homologous recombination in ES cells. The wild-type syncytin-B gene was replaced by the same gene carrying a K14R point mutation in the ISU domain. This mutation abolishes syncytin-B immunosuppressive activity without altering its fusogenic properties (ref. for the mutation: Mangeney et al, PNAS, 2007, Placental syncytins: Genetic disjunction between the fusogenic and immunosuppressive activity of retroviral envelope proteins). The targeting vector contained a 4.3-kb 5-prime arm and a 5-kb 3-prime arm corresponding to sequences bracketing the syncytin-B ORF, a 2.6 kb fragment containing the syncytin-B unique ORF into which the K14R mutation was introduced (Mangeney et al, PNAS, 2007), and the neomycin resistance (neo) gene. Syncytin-B ORF and neo gene were flanked by FRT and LoxP recombination sites, allowing their conditional excision. In the recombinant mouse strain obtained (EMMA strain ID EM:11297), the frt-flanked neo selection marker was removed by breeding with flp recombinase-expressing mice. The syncytin-B K14R mutant gene is flanked by LoxP recombination sites, allowing its conditional excision. ES cell line used: P1 [MCI-129S2/SvPas] |
Phenotypic information | Homozygous:No obvious phenotypic defects of homozygous mice (in particular, no placental phenotype). The placentation of these mice could be altered under some particular breeding conditions, due to defects in materno-fetal immune tolerance.Heterozygous:No obvious phenotypic defects of heterozygous mice. |
Breeding history | The original founder (B6;129S2/SvPas) was backcrossed 10 times to CBA/J. Then, four homozygous mutant siblings, obtained from two couples, were bred and the mutant strain subsequently maintained in a homozygous state for more than 7 generations. |
References | None available |
Homozygous fertile | yes |
Homozygous viable | yes |
Homozygous matings required | no |
Immunocompromised | not known |
Information from EMMA
Archiving centre | Institut de Transgenose, INTRAGENE, Orléans, France |
Animals used for archiving | heterozygous CBA males |
Disease and phenotype information
MGI phenotypes (gene matching)
Information on how we integrate external resources can be found here
INFRAFRONTIER® and European Mouse Mutant Archive - EMMA® are registered trademarks at the European Union Intellectual Property Office (EUIPO).