IMPC phenotypes (gene matching)
B6(C)-Cx3cr1tm1.1(cre)Jung/Orl
| Status | Available to order |
| EMMA ID | EM:06349 |
| International strain name | B6(C)-Cx3cr1tm1.1(cre)Jung/Orl |
| Alternative name | CX3CR1-Cre |
| Strain type | Targeted Mutant Strains : Knock-in |
| Allele/Transgene symbol | Cx3cr1tm1.1(cre)Jung |
| Gene/Transgene symbol | Cx3cr1 |
Information from provider
| Provider | Steffen Jung |
| Provider affiliation | Immunology, Weizmann Institute of Science |
| Genetic information | For the generation of CX3CR1-Cre mice, we employed a targeting vector carrying a 2-kb genomic fragment upstream of the Cx3cr1 start codon and a 10-kb genomic fragment downstream of the coding Cx3cr1 exon, which flanked a cre recombinase cassette gene with a floxed neomycin resistance gene. This cassette was introduced into a BAC using the RedE/T recombineering system, the Cx3cr1 coding exon was replaced with target gene; pKP-Select DK was cloned downstream of long homology arm to select against random integration. ES cells were manipulated as described previously (Jung et al., 2000). Briefly, linearized targeting vector was electroporated into C57BL/6N ES cells. Cells were positively selected for neomycin resistance. |
| Phenotypic information | CX3CR1-Cre animals harbor a targeted insertion of a cre recombinase gene into the Cx3cr1 locus. This leads to cre recombinase expression and rearrangement of loxP flanked sequences in CX3CR1 expressing cells. Of note, CX3CR1 activity and therefore cre activity in the CX3CR1-Cre animals was considered to be restricted to immune cells and in particular to the myeloid cell lineage. However, depending on which floxed allele they are crossed to, CX3CR1-Cre animals can show significant rearrangement in neurons. As adult neurons do not express CX3CR1, this is likely due to transient window of CX3CR1 promoter activity during neuronal development that so far passed unnoticed. Please be aware that this might confound your studies, in particular if they are directed at understanding microglia functions. For the latter we recommend to use the conditional TAM-dependent CX3CR1-CreER system (EM:06350). In these mice no neuronal rearrangements are detected. |
| Breeding history | Germline transmission was established on a C57BL/6 background and the mice were ever since kept on C57BL/6. To remove the neo gene they were crossed to PGK-cre mice (also on C57BL/6 background). |
| References |
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| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | Institut de Transgenose, INTRAGENE, Orléans, France |
| Animals used for archiving | homozygous C57BL/6J, wild-type C57BL/6J |
| Stage of embryos | 2-cell |
Disease and phenotype information
MGI phenotypes (allele matching)
- no phenotypic analysis / MGI
MGI phenotypes (gene matching)
- decreased monocyte cell number / MGI
- paralysis / MGI
- paresis / MGI
- demyelination / MGI
- abnormal retina morphology / MGI
- retinal degeneration / MGI
- brain inflammation / MGI
- no abnormal phenotype detected / MGI
- abnormal dendritic cell physiology / MGI
- abnormal leukocyte physiology / MGI
- no phenotypic analysis / MGI
- increased neuron apoptosis / MGI
- nervous system phenotype / MGI
- abnormal microglial cell physiology / MGI
- abnormal retinal photoreceptor layer morphology / MGI
- impaired macrophage chemotaxis / MGI
- decreased susceptibility to kidney reperfusion injury / MGI
- increased susceptibility to experimental autoimmune encephalomyelitis / MGI
- abnormal vascular wound healing / MGI
- homeostasis/metabolism phenotype / MGI
- immune system phenotype / MGI
- choroidal neovascularization / MGI
- abnormal vascular smooth muscle physiology / MGI
- abnormal response to transplant / MGI
- brainstem hemorrhage / MGI
- retinal deposits / MGI
- decreased NK cell number / MGI
- abnormal small intestinal villus morphology / MGI
- increased dendritic cell number / MGI
- thin retinal outer nuclear layer / MGI
- microgliosis / MGI
- abnormal splenocyte physiology / MGI
- increased sensitivity to induced morbidity/mortality / MGI
- increased susceptibility to bacterial infection induced morbidity/mortality / MGI
- abnormal NK cell physiology / MGI
- increased susceptibility to dopaminergic neuron neurotoxicity / MGI
Literature references
- Fate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis.;Yona Simon, Kim Ki-Wook, Wolf Yochai, Mildner Alexander, Varol Diana, Breker Michal, Strauss-Ayali Dalit, Viukov Sergey, Guilliams Martin, Misharin Alexander, Hume David A, Perlman Harris, Malissen Bernard, Zelzer Elazar, Jung Steffen, ;2013;Immunity;38;79-91; 23273845
- A new type of microglia gene targeting shows TAK1 to be pivotal in CNS autoimmune inflammation.;Goldmann Tobias, Wieghofer Peter, Müller Philippe F, Wolf Yochai, Varol Diana, Yona Simon, Brendecke Stefanie M, Kierdorf Katrin, Staszewski Ori, Datta Moumita, Luedde Tom, Heikenwalder Mathias, Jung Steffen, Prinz Marco, ;2013;Nature neuroscience;16;1618-26; 24077561
- IL-23-mediated mononuclear phagocyte crosstalk protects mice from Citrobacter rodentium-induced colon immunopathology.;Aychek Tegest, Mildner Alexander, Yona Simon, Kim Ki-Wook, Lampl Nardy, Reich-Zeliger Shlomit, Boon Louis, Yogev Nir, Waisman Ari, Cua Daniel J, Jung Steffen, ;2015;Nature communications;6;6525; 25761673
- Mertk-expressing microglia influence oligodendrogenesis and myelin modelling in the CNS.;Nguyen Linda T, Aprico Andrea, Nwoke Eze, Walsh Alexander D, Blades Farrah, Avneri Raphael, Martin Elodie, Zalc Bernard, Kilpatrick Trevor J, Binder Michele D, ;2023;Journal of neuroinflammation;20;253; 37926818