B6J.B6NCrl(Cg)-Bcl2l1tm2.2Ics/Orl
| Status | Available to order |
| EMMA ID | EM:15923 |
| Citation information | RRID:IMSR_EM:15923 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 | B6J.B6NCrl(Cg)-Bcl2l1tm2.2Ics/Orl |
| Alternative name | B6J-Bcl2l1tm2.2Ics/Orl (Mito-xL); (KIROL.KI) |
| Strain type | Targeted Mutant Strains : Knock-in |
| Allele/Transgene symbol | Bcl2l1tm2.2Ics |
| Gene/Transgene symbol | Bcl2l1 |
Information from provider
| Provider | Germain GILLET |
| Provider affiliation | Centre de Recherche en Cancérologie, Université Claude Bernard - Lyon 1 |
| Genetic information | Wild-type Bcl2l1 (Bcl-xL) protein localizes both to the endoplasmic reticulum (ER) and the mitochondria (Mito). In order to decipher the functional contribution of the ER and mitochondrial pools of Bcl-xL, we generated recombinant C57BL/6 mice by the cre recombinase-LoxP system in which Bcl-xL is exclusively at the ER (ER-xL) or at the mitochondria (Mito-xL). An engineered vector containing the wild-type Bcl-xL exon 3 and cytochrome B (CB5) or ActA mutant sequences that respectively target proteins to the ER or the mitochondria, was inserted to replace the wild-type Bcl-x exon 3 in floxed mice; cre-dependent recombination resulted in wild-type exon 3 excision and CB5 or ActA mutant expression, see references and attached documents. Accordingly, three protein products could be generated: wild-type Bcl-xL with intact transmembrane (TM) domain, ER-xL with CB5 targeting sequence, and Mito-xL with ActA targeting sequence. This strain (Mito-xL) is the post-cre mouse strain: these mice carry the ubiquitous constitutive knock-in ActA allele that targets Bcl-xL to the mitochondria, with removed antibiotics-selection cassette. Genetic background is C57BL/6J. |
| Phenotypic information | Homozygous:The homozygous mice are viable and have no identified phenotype.Heterozygous:The heterozygous mice have no identified phenotype. |
| Breeding history | Male mice carrying the conditional “floxed” ActA knock-in allele (B6-Bcl2l1tm2.1Ics/Ics; condMito-xL, KIROL.Fx; MGI:8238071; C57BL/6NCrl S3 ES cells; EMMA strain EM:16127) were crossed to C57BL/6J ubiquitous E2aCre female mice (expressing cre recombinase in oocytes). Heterozygous mice carrying the cre-recombined constitutive ActA knock-in allele were selected and backcrossed to wild-type C57BL/6J to remove the cre recombinase. Recombinase-negative heterozygous mice, carrying the cre-recombined constitutive ActA knock-in allele were selected and further backcrossed to C57BL/6J for 5 generations. |
| References |
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| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | not known |
Information from EMMA
| Archiving centre | CNRS-TAAM – Typing and Archiving of Animal Models, Orléans, France |
| Animals used for archiving | heterozygous C57BL/6J males |
Literature references
- The endoplasmic reticulum pool of Bcl-xL prevents cell death through IP3R-dependent calcium release.;Gadet Rudy, Jabbour Lea, Nguyen Trang Thi Minh, Lohez Olivier, Mikaelian Ivan, Gonzalo Philippe, Luyten Tomas, Chalabi-Dchar Mounira, Wierinckx Anne, Marcillat Olivier, Bultynck Geert, Rimokh Ruth, Popgeorgiev Nikolay, Gillet Germain, ;2024;Cell death discovery;10;346; 39090104
- Mitochondrial Bcl-xL promotes brain synaptogenesis by controlling non-lethal caspase activation.;Nguyen Trang Thi Minh, Gadet Rudy, Lanfranchi Marine, Lahaye Romane A, Yandiev Sozerko, Lohez Olivier, Mikaelian Ivan, Jabbour Lea, Rimokh Ruth, Courchet Julien, Saudou Frédéric, Popgeorgiev Nikolay, Gillet Germain, ;2023;iScience;26;106674; 37182099