IMPC phenotypes (gene matching)
129S2(B6NCrl)-Htr2btm-Lum/LumOrl
| Status | Available to order |
| EMMA ID | EM:05940 |
| Citation information | RRID:IMSR_EM:05940 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(B6NCrl)-Htr2btm-Lum/LumOrl |
| Alternative name | 5-HT2B Ex2tm2, ICS K413 L- (clone 266 -projet IR1446) |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Htr2btm-Lum |
| Gene/Transgene symbol | Htr2b |
Information from provider
| Provider | Luc Maroteaux |
| Provider affiliation | Institut du Fer a Moulin, INSERM UMR S-839 |
| Genetic information | For the gene targeting construct, a 10 kb BamHI-XhoI fragment containing the first two exons was selected, while a 4 kb SacI-SacI fragment containing exon 2, which includes the ATG start codon and 5' UTR was used to induce the targeted deletion. A loxP site was inserted in the 5'-UTR (2nd exon) and a neomycin-resistance (neo) cassette flanked by two loxP sites was inserted in the ClaI site of the second intron. Then, the SacI-SacI fragment comprising the floxed construct was excised and electroporated into 129S2 embryonic stem (ES) cells which were subjected to G418 selection. Targeted homologous recombination was confirmed by PCR and Southern blot analysis. ES cells were then transfected with cre recombinase expressing plasmid in order to eliminate the floxed locus. A positive fl- ES clone was injected into C57BL/6NCrl blastocysts and implanted into pseudopregnant mice. A chimeric male displaying germ-line transmission was then used to propagate the floxed Htr2b allele on a C57BL/6NCrl background for the first two generations. |
| Phenotypic information | The defloxed mice for the Htr2b locus constitute a new strain with total inactivation of Htr2b, targeting an exon of the gene (exon 2) different from the initial full knock-out strain (exon 3). |
| Breeding history | A positive floxed ES cell clone was injected into C57BL/6NCrl blastocysts and implanted into pseudopregnant mice. A chimeric male displaying germ-line transmission was then used to propagate the floxed Htr2b allele on a C57BL/6NCrl background for the first two generations. Seven backcrosses of Htr2b/flox mice with 129S2 wild-type mice were performed. |
| 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 | homozygous 129S2/SvPas males, wild-type 129S2/SvPas females |
| Breeding at archiving centre | Some wild-type females, provided by commercial company, potentially have a mixed background: B6.CBAx129/SvPas. It is possible that some frozen embryos have the same background. |
| Stage of embryos | 2-cell |
Disease and phenotype information
MGI phenotypes (gene matching)
- abnormal heart development / MGI
- absent trabeculae carneae / MGI
- decreased body weight / MGI
- abnormal cardiovascular system physiology / MGI
- decreased embryo size / MGI
- reduced fertility / MGI
- abnormal cardiovascular system morphology / MGI
- no abnormal phenotype detected / MGI
- disorganized myocardium / MGI
- decreased heart weight / MGI
- dilated heart atrium / MGI
- abnormal fetal cardiomyocyte proliferation / MGI
- embryonic growth retardation / MGI
- abnormal heart ventricle morphology / MGI
- cardiovascular system phenotype / MGI
- decreased right ventricle systolic pressure / MGI
- postnatal lethality, incomplete penetrance / MGI
- embryonic lethality, complete penetrance / MGI
- embryonic lethality during organogenesis, incomplete penetrance / MGI
Literature references
- Overexpression of the serotonin 5-HT2B receptor in heart leads to abnormal mitochondrial function and cardiac hypertrophy.;Nebigil Canan G, Jaffré Fabrice, Messaddeq Nadia, Hickel Pierre, Monassier Laurent, Launay Jean-Marie, Maroteaux Luc, ;2003;Circulation;107;3223-9; 12810613