IMPC phenotypes (gene matching)
- increased anti-nuclear antigen antibody level / IMPC
B6N(B6)-Trem1tm1.2Cmuel/Orl
| Status | Available to order |
| EMMA ID | EM:15810 |
| Citation information | RRID:IMSR_EM:15810 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 | B6N(B6)-Trem1tm1.2Cmuel/Orl |
| Alternative name | C57BL/6NTac-Trem1tm1.2Cmuel |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Trem1tm1.2Cmuel |
| Gene/Transgene symbol | Trem1 |
Information from provider
| Provider | Christoph Mueller |
| Provider affiliation | Institute of Tissue Medicine and Pathology, University of Bern |
| Additional owner | Prof. Mirjam Schenk, Institute of Tissue Medicine and Pathology, University of Bern, Switzerland |
| Genetic information | Trem1 knock-out. Weber B., Mueller C. in collaboration with TaconicArtemis GmbH. Electroporation of a targeting vector encoding mouse Trem1 exon 2 flanked by loxP sites into a C57BL/6NTac embryonic stem cell line. Injection of positive clones into BALB/c blastocytes and transfer to NMRI pseudopregnant females. Breeding of chimeric offspring to C57BL/6 mice. Trem1+/flox (C57BL/6-Trem1tm1821_33.1Arte) mice were further bred with mice carrying the cre recombinase under the control of the Gt(ROSA)26Sor locus to obtain systemic deletion of one Trem1 allele. Trem1+/- x cre+/- mice were interbred to achieve deletion of Cre and to obtain wild-type (Trem1+/+) and heterozygous and homozygous Trem1-deficient mice (Weber B et al., PLoS Pathog. 2014 Jan;10(1). |
| Phenotypic information | Homozygous:Animals are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No increased morbidity or mortality in naive mice. In various models of inflammation and infection, the line even showed highly attenuated disease. Full welfare assessment was performed at the University of Bern. Continuous breeding of the line between 2009 and 2014 has indicated no abnormalities in comparison to C57BL/6JRj control mice (normal fertility, no increased morbidity or mortality). Since the Trem1 knock-out line even appears to be protected in various models of inflammation and infection, the line is considered not strained.Heterozygous:Animals are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No increased morbidity or mortality in naive mice. In various models of inflammation and infection, the line even showed highly attenuated disease. Full welfare assessment was preformed at the University of Bern. Continuous breeding of the line between 2009 and 2014 has indicated no abnormalities in comparison to C57BL/6JRj control mice (normal fertility, no increased morbidity or mortality). |
| Breeding history | Trem1tm1.1Cmuel crossed to C57BL/6-Gt(ROSA)26Sortm16(Cre)Arte (TaconicArtemis) to generate the Trem1 knock-out mouse strain. The Trem1 knock-out mouse strain was generated and maintained on a C57BL/6NTac background and kept by homozygous breeding. The line has been continuously bred at the University of Bern (over 20 generations) and was cryopreserved in 2013/2014. |
| References |
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| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | yes |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | CNRS-TAAM – Typing and Archiving of Animal Models, Orléans, France |
| Animals used for archiving | homozygous C57BL/6NTac males |
Disease and phenotype information
Literature references
- TREM-1 deficiency can attenuate disease severity without affecting pathogen clearance.;Weber Benjamin, Schuster Steffen, Zysset Daniel, Rihs Silvia, Dickgreber Nina, Schürch Christian, Riether Carsten, Siegrist Mark, Schneider Christoph, Pawelski Helga, Gurzeler Ursina, Ziltener Pascal, Genitsch Vera, Tacchini-Cottier Fabienne, Ochsenbein Adrian, Hofstetter Willy, Kopf Manfred, Kaufmann Thomas, Oxenius Annette, Reith Walter, Saurer Leslie, Mueller Christoph, ;2014;PLoS pathogens;10;e1003900; 24453980