129;MF1-Igf1tm1Arge/Cnbc
| Status | Available to order |
| EMMA ID | EM:13159 |
| Citation information | RRID:IMSR_EM:13159 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 | 129;MF1-Igf1tm1Arge/Cnbc |
| Alternative name | Igf1tm1Arge_129Sv-MF1 |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Igf1tm1Arge |
| Gene/Transgene symbol | Igf1 |
Information from provider
| Provider | Isabel Varela Nieto |
| Provider affiliation | Instituto de Investigaciones Biomédicas "Alberto Sols" |
| Additional owner | Argiris Efstratiadis, MD, PhD, Biomedical Research Foundation of the Academy of Athens (BRFAA) |
| Genetic information | Replacement of sequences encoding part of exon 4 with a neomycin resistance gene. |
| Phenotypic information | Homozygous:Mutant mice lacking the Igf1 gene have severe embryonic and postnatal growth retardation that are coupled to diminished survival and delayed nerve myelination. The homozygous mutant mice maintained on a hybrid background (MF1 x 129S/Sv) present delayed inner ear development and, as a consequence, develop a profound syndromic sensorineural hearing loss with increased hearing thresholds.Heterozygous:The young heterozygous mice present normal hearing and show no evident cellular alterations. |
| Breeding history | The mice were obtained by backcrossing the original line on MF1 x 129S/Sv background (Liu et al., 1993, doi: 10.1016/S0092-8674(05)80084-4), selected because of the increased survival of the homozygous mutant progeny. The original mutant line was firstly backcrossed to the MF1 background at least 10 times, and 2 more times in the last 10 years to the 129S/SvEv background. Wild-type males and females were used. |
| References |
|
| Homozygous fertile | no |
| 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 129S/SvEv x MF1 males |
Disease and phenotype information
Orphanet associated rare diseases, based on orthologous gene matching
- Growth delay due to insulin-like growth factor type 1 deficiency / Orphanet_73272
Literature references
- A comparative study of age-related hearing loss in wild type and insulin-like growth factor I deficient mice.;Riquelme Raquel, Cediel Rafael, Contreras Julio, la Rosa Lourdes Rodriguez-de, Murillo-Cuesta Silvia, Hernandez-Sanchez Catalina, Zubeldia Jose M, Cerdan Sebastian, Varela-Nieto Isabel, ;2010;Frontiers in neuroanatomy;4;27; 20661454
- RNA microarray analysis in prenatal mouse cochlea reveals novel IGF-I target genes: implication of MEF2 and FOXM1 transcription factors.;Sanchez-Calderon Hortensia, Rodriguez-de la Rosa Lourdes, Milo Marta, Pichel Jose G, Holley Matthew, Varela-Nieto Isabel, ;2010;PloS one;5;e8699; 20111592
- Delayed inner ear maturation and neuronal loss in postnatal Igf-1-deficient mice.;Camarero G, Avendano C, Fernandez-Moreno C, Villar A, Contreras J, de Pablo F, Pichel J G, Varela-Nieto I, ;2001;The Journal of neuroscience : the official journal of the Society for Neuroscience;21;7630-41; 11567053
- Sensorineural hearing loss in insulin-like growth factor I-null mice: a new model of human deafness.;Cediel R, Riquelme R, Contreras J, Díaz A, Varela-Nieto I, ;2006;The European journal of neuroscience;23;587-90; 16420467
- Mice carrying null mutations of the genes encoding insulin-like growth factor I (Igf-1) and type 1 IGF receptor (Igf1r).;Liu J P, Baker J, Perkins A S, Robertson E J, Efstratiadis A, ;1993;Cell;75;59-72; 8402901