IMPC phenotypes (gene matching)
B6.129(C)-Cx3cr1tm2.1(cre/ERT2)Jung/Orl
| Status | Available to order |
| EMMA ID | EM:06350 |
| International strain name | B6.129(C)-Cx3cr1tm2.1(cre/ERT2)Jung/Orl |
| Alternative name | CX3CR1-CreER |
| Strain type | Targeted Mutant Strains : Knock-in |
| Allele/Transgene symbol | Cx3cr1tm2.1(cre/ERT2)Jung |
| Gene/Transgene symbol | Cx3cr1 |
Information from provider
| Provider | Steffen Jung |
| Provider affiliation | Immunology, Weizmann Institute of Science |
| Genetic information | For the generation of the CX3CR1-CreER mice the homologous regions of the vector contained a 1.2 kb fragment upstream of the Cx3cr1 start codon (Short Homology) and an 8 kb fragment spanning the 3' end of the Cx3cr1 coding exon (Long Homology). The CreERT2 cassette gene, a kind gift of D. Metzger (Indra et al., 1999), and loxP flanked neomycin resistance gene were introduced replacing the first 390 bp of the Cx3cr1 gene, a HSV-tk gene was cloned downstream of the LH to select against random integration (Jung et al., 2000). ES cells were manipulated as described previously (Jung et al., 2000). Briefly, linearized targeting vector was electroporated into ES cells (129 R1 cells). CX3CR1CreER ES cells were negatively selected against random integration by the addition of ganciclovir. Cells were positively selected for neomycin resistance with G418 (200 µg/ml) and resistant colonies were isolated and analyzed for homologous recombination by PCR. |
| Phenotypic information | CX3CR1-CreER mice harbor a gene encoding a cre recombinase-estrogen receptor fusion. This leads in Cx3cr1 expressing cells to latent cre activity that can be activated by tamoxifen administration. |
| Breeding history | The strain was backcrossed more than 10 generations to C57BL/6 and the neo gene was removed by a cross to PGK-cre transgenic mice (also on C57BL/6). |
| References |
|
| 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 |
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
- Microglial-glucocorticoid receptor depletion alters the response of hippocampal microglia and neurons in a chronic unpredictable mild stress paradigm in female mice.;Picard Katherine, Bisht Kanchan, Poggini Silvia, Garofalo Stefano, Golia Maria Teresa, Basilico Bernadette, Abdallah Fatima, Ciano Albanese Naomi, Amrein Irmgard, Vernoux Nathalie, Sharma Kaushik, Hui Chin Wai, C Savage Julie, Limatola Cristina, Ragozzino Davide, Maggi Laura, Branchi Igor, Tremblay Marie-Ève, ;2021;Brain, behavior, and immunity;97;423-439; 34343616
- The alarmin interleukin-1α triggers secondary degeneration through reactive astrocytes and endothelium after spinal cord injury.;Bretheau Floriane, Castellanos-Molina Adrian, Bélanger Dominic, Kusik Maxime, Mailhot Benoit, Boisvert Ana, Vallières Nicolas, Lessard Martine, Gunzer Matthias, Liu Xiaoyu, Boilard Éric, Quan Ning, Lacroix Steve, ;2022;Nature communications;13;5786; 36184639
- Myeloid cell transmigration across the CNS vasculature triggers IL-1β-driven neuroinflammation during autoimmune encephalomyelitis in mice.;Lévesque Sébastien A, Paré Alexandre, Mailhot Benoit, Bellver-Landete Victor, Kébir Hania, Lécuyer Marc-André, Alvarez Jorge Ivan, Prat Alexandre, de Rivero Vaccari Juan Pablo, Keane Robert W, Lacroix Steve, ;2016;The Journal of experimental medicine;213;929-49; 27139491