STOCK Fzd9tm1Sjp/Cnbc
| Status | Available to order |
| EMMA ID | EM:14602 |
| Citation information | RRID:IMSR_EM:14602 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 | STOCK Fzd9tm1Sjp/Cnbc |
| Alternative name | Fzd9KO/KO |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Fzd9tm1Sjp |
| Gene/Transgene symbol | Fzd9 |
Information from provider
| Provider | Samuel Pleasure |
| Provider affiliation | University of California San Francisco (UCSF) |
| Genetic information | The Fzd9 KO/KO mice were originally obtained from Zhao et al. 2005, who generated the line as follows: A mouse frizzled class receptor 9 (Fzd9) genomic clone was obtained from a 129/SvJ library. The entire 1.8 kb Fzd9 coding region was replaced by IRES-lacZ-loxP-PGKneo-loxP selection cassette, and the electroporation was performed using standard procedures. Homologous recombinant clones were identified by Southern blot. The targeted ES clones were injected into C57BL/6J blastocysts and chimeric mice were bred with C57BL/6J females. Fzd9 mutants were obtained from heterozygous intercrosses. |
| Phenotypic information | Homozygous:Fzd9 null mice had generally normal gross anatomical hippocampal organization but showed large increases in apoptotic cell death in the developing dentate gyrus. This increase in programmed cell death commenced with the onset of dentate gyrus development and persisted into the first postnatal week of life. There was also a perhaps compensatory increase in the number of dividing precursors in the dentate gyrus. These changes in the mutants resulted in a moderate decrease in the number of adult dentate granule cells in null mice and an increase in the number of hilar mossy cells. All mice with a mutant allele had diminished seizure thresholds, and Fzd9 null mice had severe deficits on tests of visuospatial learning/memory. In an unrelated, independent study (Ranheim et al. 2005) using Fzd KO/KO mice from a different colony, the authors identified abnormalities in B-cell development. Briefly, this study reported that Fzd9-/- mice show no obvious features of Williams-Beuren syndrome, but reveal a role for Fzd9 in lymphoid development and maturation. Fzd9-/- mice show pronounced splenomegaly, thymic atrophy, and lymphadenopathy with age, with accumulation of plasma cells in lymph nodes. There is a depletion of developing B cells in the bone marrow (BM), particularly in the pre-B stage where immunoglobulin heavy chains are expressed and the cells are undergoing clonal expansion prior to light chain rearrangement. The pre-B defect is partially intrinsic to the hematopoietic system; as in competitive BM reconstitution studies, Fzd9 null-derived BM exhibits defective B-cell development when implanted into a wild-type host. Mature B cells are present in normal numbers in lymph node and spleen.Heterozygous:Heterozygous mice (the same frizzled 9 genotype as Williams-Beuren syndrome patients) were intermediate between wild-type and null mice for all developmental neuronanatomic defects. All mice with a mutant allele had diminished seizure thresholds, and Fzd9 null mice had severe deficits on tests of visuospatial learning/memory. |
| Breeding history | The animals obtained were crossed with pIns-MycERTAM;RIP7-Bcl-xL transgenic mice (Finch et al. 2006) and the pIns-MycERTAM;RIP7-Bcl-xL;Fzd9 KO/KO colony was maintained through repeated crossing until 05/2021. Starting from 05/2021, mice heterozygous or homozygous for Fzd KO and wild-type for pIns-MycERTAM;RIP7-Bcl-xL were crossed to generate Fzd9 KO/KO mice for freezing. |
| References |
|
| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | CNB-CSIC, Centro Nacional de Biotecnologia, Madrid, Spain |
| Animals used for archiving | heterozygous C57BL/6J males |
Literature references
- Frizzled 9 knock-out mice have abnormal B-cell development.;Ranheim Erik A, Kwan Helen C K, Reya Tannishtha, Wang Yu-Ker, Weissman Irving L, Francke Uta, ;2005;Blood;105;2487-94; 15572594
- Hippocampal and visuospatial learning defects in mice with a deletion of frizzled 9, a gene in the Williams syndrome deletion interval.;Zhao Chunjie, Avilés Carmen, Abel Regina A, Almli C Robert, McQuillen Patrick, Pleasure Samuel J, ;2005;Development (Cambridge, England);132;2917-27; 15930120