MGI phenotypes (allele matching)
129S2(B6)-Meg3Gt(pGTi)216Gos/H
| Status | Available to order |
| EMMA ID | EM:06878 |
| Citation information | RRID:IMSR_EM:06878 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 | 129S2(B6)-Meg3Gt(pGTi)216Gos/H |
| Alternative name | Gtl2LacZ |
| Strain type | Gene-trap |
| Allele/Transgene symbol | Meg3Gt(pGTi)216Gos |
| Gene/Transgene symbol | Meg3 |
Information from provider
| Provider | Karin Schuster-Gossler |
| Provider affiliation | Medizinische Hochschule Hannover, Institute for Molecular Biology |
| Additional owner | Dr. Anne Ferguson-Smith |
| Genetic information | Gene-trap insertion 2kb upstream of Meg3. Disrupts imprinted gene expression of multiple genes in cis. |
| Phenotypic information | Imprinted dwarfism and thyroid hormone defects. This transgenic mouse line carries an insertional mutation with a dominant modified pattern of inheritance: heterozygous Meg3 (or Gtl2) lacZ mice that inherited the transgene from the father show a proportionate dwarfism phenotype; whereas the penetrance and expressivity of the phenotype is strongly reduced in Gtl2 lacZ mice that inherited the transgene from the mother. On a mixed genetic background this pattern of inheritance was reversible upon transmission of the transgene through the germ line of the opposite sex whereas on a predominantly 129S2/SvPas genetic background the transgene passage through the female germ line modifies the transgene effect, such that the penetrance of the mutation was drastically reduced and the phenotype is no longer obvious after subsequent male germ line transmission. Expression of the transgene is neither affected by genetic background nor by parental legacy. It has been postulated that that the transgene insertion in Gtl2 lacZ mice affects an endogenous gene(s) required for fetal and postnatal growth and that this gene(s) is predominantly paternally expressed. |
| Breeding history | The 129/Sv derived ES cell line D3/GT 216, which carries the gene trap vector pGti integrated into its genome, was injected into C57BL/6 blastocysts. Male chimeras were mated to C57BL/6 females. Mice were received on a C57BL/6 background and were backcrossed onto 129S2/SvPas for >5 generations, then maintained as an inbred stock. |
| References |
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| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | Mary Lyon Centre at MRC Harwell, Oxford, United Kingdom |
Disease and phenotype information
MGI phenotypes (gene matching)
- abnormal muscle development / MGI
- decreased body weight / MGI
- decreased body size / MGI
- hepatic necrosis / MGI
- postnatal growth retardation / MGI
- respiratory failure / MGI
- postnatal lethality / MGI
- premature death / MGI
- abnormal pulmonary alveolus morphology / MGI
- disproportionate dwarf / MGI
- abnormal skeletal muscle fiber morphology / MGI
- maternal imprinting / MGI
- paternal imprinting / MGI
- abnormal imprinting / MGI
- fetal growth retardation / MGI
- decreased placenta weight / MGI
- growth/size/body region phenotype / MGI
- embryo phenotype / MGI
- cellular phenotype / MGI
- decreased survivor rate / MGI
- decreased fetal weight / MGI
- mortality/aging / MGI
- postnatal lethality, incomplete penetrance / MGI
- neonatal lethality, incomplete penetrance / MGI
- perinatal lethality, complete penetrance / MGI
- prenatal lethality, incomplete penetrance / MGI
Literature references
- Gtl2lacZ, an insertional mutation on mouse chromosome 12 with parental origin-dependent phenotype.;Schuster-Gossler K, Simon-Chazottes D, Guenet J L, Zachgo J, Gossler A, ;1996;Mammalian genome : official journal of the International Mammalian Genome Society;7;20-4; 8903723
- Imprinted gene dosage is critical for the transition to independent life.;Charalambous Marika, Ferron Sacramento R, da Rocha Simao T, Murray Andrew J, Rowland Timothy, Ito Mitsuteru, Schuster-Gossler Karin, Hernandez Arturo, Ferguson-Smith Anne C, ;2012;Cell metabolism;15;209-21; 22326222
- Loss of imprinting at the Dlk1-Gtl2 locus caused by insertional mutagenesis in the Gtl2 5' region.;Steshina Ekaterina Y, Carr Michael S, Glick Elena A, Yevtodiyenko Aleksey, Appelbe Oliver K, Schmidt Jennifer V, ;2006;BMC genetics;7;44; 17014736