FVB.129P2-Igf2rtm2Wag/Biat
Status | Available to order |
EMMA ID | EM:09897 |
Citation information | RRID:IMSR_EM:09897 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 | FVB.129P2-Igf2rtm2Wag/Biat |
Alternative name | FVB.129P2-Airn-R2D (FVB.129P2- Igf2r |
Strain type | Targeted Mutant Strains : Other targeted |
Allele/Transgene symbol | Igf2rtm2Wag |
Gene/Transgene symbol | Igf2r |
Information from provider
Provider | Denise Barlow |
Provider affiliation | CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences |
Genetic information | The R2D allele has a 3.6kb deletion (chr17:12,740,792-12,744,359, GRCm38/mm10) that includes the Airn promoter and the imprint control element (ICE) of the Igf2r imprinted cluster, with 95 bp vector remaining, including a single loxP site. The deletion was created in E14 ES cells (129P2/OlaHsd), which were then used to make chimeras with C57BL/6 blastocysts. The allele has been backcrossed to FVB/N for over 50 generations. |
Phenotypic information | Homozygous:Homozygous R2D mice are viable and fertile, but show reduced embryonic and neonatal growth due to biallelic expression of Igf2r due to the deletion of the Airn promoter and loss of imprinted silencing of Igf2r on the paternal allele.Heterozygous:Heterozygous R2D mice are viable and fertile, but mice that inherit the deletion paternally have a loss of Igf2r imprinted expression and the reduced growth phenotype described for the homozygous mice. Mice that inherit the R2D allele maternally show no phenotype. |
Breeding history | R2D mice were derived from 129/Sv x C57BL/6 chimeras and then backcrossed to FVB/N for over 50 generations. |
References |
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Homozygous fertile | yes |
Homozygous viable | yes |
Homozygous matings required | no |
Immunocompromised | no |
Information from EMMA
Archiving centre | University of Veterinary Medicine, Vienna, Austria |
Animals used for archiving | heterozygous FVB/N males |
Disease and phenotype information
MGI phenotypes (allele matching)
MGI phenotypes (gene matching)
- enlarged heart / MGI
- heart hyperplasia / MGI
- abnormal interventricular septum morphology / MGI
- abnormal craniofacial morphology / MGI
- polydactyly / MGI
- kinked tail / MGI
- short tail / MGI
- enlarged liver / MGI
- abnormal body water content / MGI
- abnormal uterus morphology / MGI
- vagina atresia / MGI
- abnormal lung morphology / MGI
- abnormal lung development / MGI
- increased body weight / MGI
- increased body size / MGI
- absent suckling reflex / MGI
- cyanosis / MGI
- increased embryo size / MGI
- edema / MGI
- reduced male fertility / MGI
- reduced female fertility / MGI
- female infertility / MGI
- decreased litter size / MGI
- respiratory failure / MGI
- respiratory distress / MGI
- abnormal motor capabilities/coordination/movement / MGI
- abnormal embryonic growth/weight/body size / MGI
- disorganized myocardium / MGI
- abnormal tricuspid valve morphology / MGI
- dilated heart left ventricle / MGI
- dilated heart right ventricle / MGI
- increased heart weight / MGI
- thick ventricular wall / MGI
- enlarged kidney / MGI
- genetic imprinting / MGI
- maternal imprinting / MGI
- abnormal external female genitalia morphology / MGI
- abnormal lysosome physiology / MGI
- premature bone ossification / MGI
- increased fetal size / MGI
- pulmonary hyperplasia / MGI
- enlarged placenta / MGI
- split sternum / MGI
- short sternum / MGI
- enlarged lung / MGI
- enlarged uterus / MGI
- increased placenta weight / MGI
- dilated heart / MGI
- liver hyperplasia / MGI
- increased brain size / MGI
- abnormal myocardium layer morphology / MGI
- homeostasis/metabolism phenotype / MGI
- growth/size/body region phenotype / MGI
- reproductive system phenotype / MGI
- abnormal circulating hormone level / MGI
- congestive heart failure / MGI
- thin endometrium / MGI
- abnormal bone ossification / MGI
- decreased survivor rate / MGI
- increased heart ventricle size / MGI
- abnormal uterine horn morphology / MGI
- dilated uterine horn / MGI
- absent endometrial glands / MGI
- increased nucleated erythrocyte cell number / MGI
- decreased fetal weight / MGI
- increased fetal weight / MGI
- increased birth weight / MGI
- heart hemorrhage / MGI
- increased birth body size / MGI
- increased heart right ventricle size / MGI
- thick interventricular septum / MGI
- mortality/aging / MGI
- impaired branching involved in preterminal bronchiole morphogenesis / MGI
- postnatal lethality, complete penetrance / MGI
- postnatal lethality, incomplete penetrance / MGI
- neonatal lethality, complete penetrance / MGI
- neonatal lethality, incomplete penetrance / MGI
- perinatal lethality, incomplete penetrance / MGI
- prenatal lethality, complete penetrance / MGI
- lethality throughout fetal growth and development, incomplete penetrance / MGI
- preweaning lethality, incomplete penetrance / MGI
- enlarged uterine horn / MGI
Literature references
- Non-imprinted Igf2r expression decreases growth and rescues the Tme mutation in mice.;Wutz A, Theussl H C, Dausman J, Jaenisch R, Barlow D P, Wagner E F, ;2001;Development (Cambridge, England);128;1881-7; 11311167
- Bidirectional action of the Igf2r imprint control element on upstream and downstream imprinted genes.;Zwart R, Sleutels F, Wutz A, Schinkel A H, Barlow D P, ;2001;Genes & development;15;2361-6; 11562346
- Airn transcriptional overlap, but not its lncRNA products, induces imprinted Igf2r silencing.;Latos Paulina A, Pauler Florian M, Koerner Martha V, Şenergin H Başak, Hudson Quanah J, Stocsits Roman R, Allhoff Wolfgang, Stricker Stefan H, Klement Ruth M, Warczok Katarzyna E, Aumayr Karin, Pasierbek Pawel, Barlow Denise P, ;2012;Science (New York, N.Y.);338;1469-72; 23239737
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