IMPC phenotypes (gene matching)
B6J;129S2-Magel2tm1.1Mus/Orl
| Status | Available to order |
| EMMA ID | EM:15286 |
| Citation information | RRID:IMSR_EM:15286 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;129S2-Magel2tm1.1Mus/Orl |
| Alternative name | Magel2 tm1.1Mus-knockout mouse |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Magel2tm1.1Mus |
| Gene/Transgene symbol | Magel2 |
Information from provider
| Provider | Françoise Muscatelli |
| Provider affiliation | INSERM UMR1249, Institut de Neurobiologie de la Méditerranée (INMED) |
| Genetic information | Deletion of Magel2 gene promoter and coding sequence for the N-terminal part of MAGEL2 protein. Homologous recombination in ES cells. ES clones were electroporated with a cre recombinase-expressing vector. ES cell clones carrying the allele in which the hygromycin resistance gene had been deleted were selected by PCR. |
| Phenotypic information | Homozygous:Similar to the heterozygous when the mutation is on the paternal allele since Magel2 is an imprinted gene with paternal expression; the maternal allele is silent. Heterozygous:Magel2 is an imprinted gene whose expression is only paternal. Heterozygous mice with a deletion on the paternal allele (and a wild-type maternal allele) are considered knock-out mice. These mice are viable and fertile (if mated at less than 4 months). After birth, the pups suffer from suckling deficit that can lead to death of some pups. Sensory problems have been detected from the first week of life. In adulthood, social and cognitive impairments have been described (Schaller F, Watrin F, Sturny R, Massacrier A, Szepetowski P, Muscatelli F. A single postnatal injection of oxytocin rescues the lethal feeding behaviour in mouse newborns deficient for the imprinted Magel2 gene. Hum Mol Genet 2010; 19(24): 4895-4905). |
| Breeding history | Generated on the C57BL/6J genetic background and maintained on this background. |
| References |
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| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | CNRS-TAAM – Typing and Archiving of Animal Models, Orléans, France |
| Animals used for archiving | heterozygous C57BL/6J males |
Disease and phenotype information
Literature references
- The impact of oxytocin on neurite outgrowth and synaptic proteins in Magel2-deficient mice.;Reichova Alexandra, Schaller Fabienne, Bukatova Stanislava, Bacova Zuzana, Muscatelli Françoise, Bakos Jan, ;2021;Developmental neurobiology;81;366-388; 33609001
- Early life oxytocin treatment improves thermo-sensory reactivity and maternal behavior in neonates lacking the autism-associated gene Magel2.;Da Prato Laura Caccialupi, Zayan Ugo, Abdallah Dina, Point Vanessa, Schaller Fabienne, Pallesi-Pocachard Emilie, Montheil Aurélie, Canaan Stéphane, Gaiarsa Jean-Luc, Muscatelli Françoise, Matarazzo Valéry, ;2022;Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology;47;1901-1912; 35396500
- An Early Postnatal Oxytocin Treatment Prevents Social and Learning Deficits in Adult Mice Deficient for Magel2, a Gene Involved in Prader-Willi Syndrome and Autism.;Meziane Hamid, Schaller Fabienne, Bauer Sylvian, Villard Claude, Matarazzo Valery, Riet Fabrice, Guillon Gilles, Lafitte Daniel, Desarmenien Michel G, Tauber Maithé, Muscatelli Françoise, ;2015;Biological psychiatry;78;85-94; 25599930
- A single postnatal injection of oxytocin rescues the lethal feeding behaviour in mouse newborns deficient for the imprinted Magel2 gene.;Schaller Fabienne, Watrin Françoise, Sturny Rachel, Massacrier Annick, Szepetowski Pierre, Muscatelli Françoise, ;2010;Human molecular genetics;19;4895-905; 20876615
- Oxytocin administration in neonates shapes hippocampal circuitry and restores social behavior in a mouse model of autism.;Bertoni Alessandra, Schaller Fabienne, Tyzio Roman, Gaillard Stephane, Santini Francesca, Xolin Marion, Diabira Diabé, Vaidyanathan Radhika, Matarazzo Valery, Medina Igor, Hammock Elizabeth, Zhang Jinwei, Chini Bice, Gaiarsa Jean-Luc, Muscatelli Françoise, ;2021;Molecular psychiatry;26;7582-7595; 34290367