Analysis Tools
homeostasis/metabolism
| N |
• mice exhibit normal response (dopamine nerve loss, increased body temperature, and microgliosis) to methamphetamine treatment
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Allele Symbol Allele Name Allele ID |
Cx3cr1tm1Litt targeted mutation 1, Dan R Littman MGI:2670351 |
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| Summary |
14 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice exhibit normal response (dopamine nerve loss, increased body temperature, and microgliosis) to methamphetamine treatment
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following induction of experimental autoimmune encephalomyelitis
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• mice show numerous white/yellow fundus lesions at 16 months of age but not at 3 months
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• marker analysis indicates that photoreceptor maturation is abnormal with impaired outer segment elongation
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• overall cilium structure is unaffected, however cilium proteins show altered distribution in the transitional zone during photoreceptor maturation
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• cone number is reduced from P30 in the periphery and in the central retina at P90
• however, outer nuclear layer thickness is not altered in either the peripheral or central retina
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• mice show shortened outer segments in P21 retina
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• from P30 on
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• microglial processes are often seen extending deep into the outer nuclear layer where photoreceptors reside
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• cell loss is seen in the outer nuclear layer of 16 month old retina but not 3 month old retina
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• late-stage retinal degeneration
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• retina shows increased Muller cell gliosis from around eye opening at P14, becoming significant from 1 month of age, and extensive gliosis, particularly within the inner plexiform layer at 3 months of age
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• 22% decrease in amplitude of the a-wave at P270 but not earlier, indicating a late onset of reduced rod-related function
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• cone-related function is reduced from P17, shows no increase in response coincident with photoreceptor maturation, the functional deficit remains at P30 and P90, while no difference is seen at P270, with a decrease in b wave amplitude at P17, P30, and P90
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• following induction of experimental autoimmune encephalomyelitis
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• following LPS exposure, neuron apoptosis is increased unlike in heterozygous mice
• LPS-induced neurotoxicity is cell-autonomous
• however, mice subjected to adoptive transfer experiments and treated with an IL1 receptor antagonist exhibit reduced neuron apoptosis
• however, adoptive transfer into Il1r null mice abolishes neuron apoptosis
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• mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exhibit more severe neurotoxicity than similarly treated wild-type mice
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• increase in microglia numbers in the outer nuclear layer from P14 and a trend for increased microglial process number from P14 becoming significant at P90
• presence of microglial processes in the outer retinal is increased at P14 compared with P90, with levels further increased at P270
• microglia at the level of the photoreceptor terminals exhibit normal soma size and process number with increased process length, indicating that microglia are not classically activated
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• intense and widespread following LPS exposure
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• migration of microglial cells in LPS-treated mice is impaired unlike in similarly treated heterozygous mice
(J:110266)
• however, adoptive transfer into Il1r null mice restores microglial cell migration
(J:110266)
• microglial-cone interactions are increased in the central and peripheral retina at P21
(J:265696)
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• following induction of experimental autoimmune encephalomyelitis
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• marker analysis indicates that photoreceptor maturation is abnormal with impaired outer segment elongation
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• overall cilium structure is unaffected, however cilium proteins show altered distribution in the transitional zone during photoreceptor maturation
|
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• cone number is reduced from P30 in the periphery and in the central retina at P90
• however, outer nuclear layer thickness is not altered in either the peripheral or central retina
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• mice show shortened outer segments in P21 retina
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• from P30 on
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• following induction of experimental autoimmune encephalomyelitis, mice exhibit more severe demyelination compared with similarly treated wild-type mice
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| N |
• mice exhibit normal response to murine cytomegalovirus infection
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• in the central nervous system following induction of experimental autoimmune encephalomyelitis
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• increase in microglia numbers in the outer nuclear layer from P14 and a trend for increased microglial process number from P14 becoming significant at P90
• presence of microglial processes in the outer retinal is increased at P14 compared with P90, with levels further increased at P270
• microglia at the level of the photoreceptor terminals exhibit normal soma size and process number with increased process length, indicating that microglia are not classically activated
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• intense and widespread following LPS exposure
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• following arterial injury, monocyte recruitment is impaired compared to in similarly treated wild-type mice
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• following induction of experimental autoimmune encephalomyelitis, recruitment of NK cells is impaired compared to in similarly treated wild-type mice
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• migration of microglial cells in LPS-treated mice is impaired unlike in similarly treated heterozygous mice
(J:110266)
• however, adoptive transfer into Il1r null mice restores microglial cell migration
(J:110266)
• microglial-cone interactions are increased in the central and peripheral retina at P21
(J:265696)
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• following induction of experimental autoimmune encephalomyelitis, mice exhibit earlier onset, higher mortality, and more severe EAE symptoms (nonremitting spastic paralysis, increased hemorrhagic inflammation, and extensive demyelination) compared with similarly treated wild-type mice
• following induction of experimental autoimmune encephalomyelitis, recruitment of NK cells is impaired compared to in similarly treated wild-type mice
• however, priming of encephalitogenic T cells and NKT cell numbers are normal
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• following induction of experimental autoimmune encephalomyelitis
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• following induction of experimental autoimmune encephalomyelitis
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• following arterial injury, vascular smooth muscle cell proliferation is decreased compared to in similarly treated wild-type mice
• in vitro, vascular smooth muscle cells fail to proliferate in response to CXCL1 unlike similarly treated wild-type cells
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• following arterial injury, mice exhibit decreased intimal hyperplasia, impaired monocyte recruitment into the vascular wall, and decreased vascular smooth muscle cell proliferation compared to in similarly treated wild-type mice
• however, mice exhibit normal luminal and medial areas and platelet function
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• following arterial injury, mice exhibit decreased intimal hyperplasia, impaired monocyte recruitment into the vascular wall, and decreased vascular smooth muscle cell proliferation compared to in similarly treated wild-type mice
• however, mice exhibit normal luminal and medial areas and platelet function
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• mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exhibit more severe neurotoxicity than similarly treated wild-type mice
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• following induction of experimental autoimmune encephalomyelitis, mice exhibit nonremitting spastic paralysis
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• in the central nervous system following induction of experimental autoimmune encephalomyelitis
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• increase in microglia numbers in the outer nuclear layer from P14 and a trend for increased microglial process number from P14 becoming significant at P90
• presence of microglial processes in the outer retinal is increased at P14 compared with P90, with levels further increased at P270
• microglia at the level of the photoreceptor terminals exhibit normal soma size and process number with increased process length, indicating that microglia are not classically activated
|
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• intense and widespread following LPS exposure
|
|
• following arterial injury, monocyte recruitment is impaired compared to in similarly treated wild-type mice
|
|
• following induction of experimental autoimmune encephalomyelitis, recruitment of NK cells is impaired compared to in similarly treated wild-type mice
|
|
• migration of microglial cells in LPS-treated mice is impaired unlike in similarly treated heterozygous mice
(J:110266)
• however, adoptive transfer into Il1r null mice restores microglial cell migration
(J:110266)
• microglial-cone interactions are increased in the central and peripheral retina at P21
(J:265696)
|
|
• following arterial injury, vascular smooth muscle cell proliferation is decreased compared to in similarly treated wild-type mice
• in vitro, vascular smooth muscle cells fail to proliferate in response to CXCL1 unlike similarly treated wild-type cells
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• following arterial injury, vascular smooth muscle cell proliferation is decreased compared to in similarly treated wild-type mice
• in vitro, vascular smooth muscle cells fail to proliferate in response to CXCL1 unlike similarly treated wild-type cells
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• overall cilium structure is unaffected, however cilium proteins show altered distribution in the transitional zone during photoreceptor maturation
|
|
• following LPS exposure, neuron apoptosis is increased unlike in heterozygous mice
• LPS-induced neurotoxicity is cell-autonomous
• however, mice subjected to adoptive transfer experiments and treated with an IL1 receptor antagonist exhibit reduced neuron apoptosis
• however, adoptive transfer into Il1r null mice abolishes neuron apoptosis
|
|
• mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exhibit more severe neurotoxicity than similarly treated wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• normal monocyte extravasation and subsequent differentiation into macrophages in response to intraperitoneal injection of thioglycolate, a model of acute peritonitis
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• S. typhimurium-infected mice exhibit a higher organ bacterial load and die within 6 days of infection unlike similarly treated heterozygous and wild-type mice
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• antibiotic-treated mice exhibit increased numbers of all subsets of dendritic cells in the mesenteric lymph nodes as compared to untreated controls
• mice treated with antibiotic and infected with non-invasive Salmonella exhibit increased numbers of only CX3CR1
cells in the mesenteric lymph nodes and afferent lymph nodes as compared to uninfected controls
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• laminar propria dendritic cells exhibit impaired capacity to traverse the epithelial cell monolayer unlike in heterozygous mice
(J:95694)
• laminar propria dendritic cells fail to properly sample E. coli unlike in heterozygous mice
(J:95694)
• ileal villi lack intraepithelial dendritic cell extensions unlike in heterozygous mice
(J:95694)
• S. typhimurium-infected mice exhibit laminar propria dendritic cells that only form globular structures that fail to cross the epithelium unlike in similarly treated heterozygous mice
(J:95694)
• however, sampling of E. coli into the Peyer Patches is normal
(J:95694)
• intestinal CX3CR1+ cells show defective dendrite extension after treatment with lactic or pyruvic acid
(J:271242)
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• intestinal CX3CR1+ cells show defective dendrite extension after treatment with lactic or pyruvic acid
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• S. typhimurium-infected mice exhibit a higher organ bacterial load and die within 6 days of infection unlike similarly treated heterozygous and wild-type mice
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• ileal villi lack intraepithelial dendritic cell extensions unlike in heterozygous mice
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• antibiotic-treated mice exhibit increased numbers of all subsets of dendritic cells in the mesenteric lymph nodes as compared to untreated controls
• mice treated with antibiotic and infected with non-invasive Salmonella exhibit increased numbers of only CX3CR1
cells in the mesenteric lymph nodes and afferent lymph nodes as compared to uninfected controls
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• normal dendritic cell migration and IL-12 production in response to a microbial antigen (STAg)
• normal Langerhans cell migration and APC function in response to contact sensitizer (oxazolone)
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• mice exhibit a reduction in the number of total monocytes compared with wild-type mice
• Gr1low monocytes are reduced 3-fold compared to in wild-type mice
• however, expression of Tg(S100A8-BCL2)1Lgs restores monocyte numbers
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• following kidney ischemia and reperfusion, mice exhibit reduced monocyte egress from the blood into the inflamed kidney compared with similarly treated wild-type mice
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• following kidney ischemia and reperfusion
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• following kidney ischemia and reperfusion, mice exhibit decreased kidney injury, tubular cell necrosis, and macrophage recruitment compared with similarly treated heterozygous mice
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• following laser injury, more subretinal microglial cells accumulate adjacent to the choroid scar than in similarly treated wild-type mice and choroid neovascularization is twice as much as in similarly treated wild-type mice
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• subretinal microglial cells accumulate with age in the retina unlike in wild-type mice
• following laser injury, more subretinal microglial cells accumulate adjacent to the choroid scar than in heterozygous mice at 7 and 14 days post injury
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• following kidney ischemia and reperfusion, mice exhibit decreased kidney injury, tubular cell necrosis, and macrophage recruitment compared with similarly treated heterozygous mice
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| N |
• normal neuronal-glial cross talk indicated by microglial response to peripheral nerve injury, 129P2/OlaHsd and C57BL/6 mixed genetic background
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• following laser injury, more subretinal microglial cells accumulate adjacent to the choroid scar than in similarly treated wild-type mice and choroid neovascularization is twice as much as in similarly treated wild-type mice
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• mice exhibit a reduction in the number of total monocytes compared with wild-type mice
• Gr1low monocytes are reduced 3-fold compared to in wild-type mice
• however, expression of Tg(S100A8-BCL2)1Lgs restores monocyte numbers
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• following kidney ischemia and reperfusion, mice exhibit reduced monocyte egress from the blood into the inflamed kidney compared with similarly treated wild-type mice
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• following kidney ischemia and reperfusion
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• following kidney ischemia and reperfusion
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• moderate following LPS exposure
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• moderate following LPS exposure
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• following induction of experimental autoimmune encephalomyelitis (EAE), mice exhibit intermediate EAE severity (including transient flaccid paresis) compared with homozygous and wild-type mice
• mice treated with anti-NK1.1 antibodies exhibit the same severity of EAE as in homozygous mice following induction of experimental autoimmune encephalomyelitis
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• following induction of experimental autoimmune encephalomyelitis, mice exhibit transient flaccid paresis
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• moderate following LPS exposure
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following induction of experimental autoimmune encephalomyelitis (EAE), mice exhibit a similar reduction in NK1.1/TCRbeta- cells in the central nervous system observed in similarly treated Cx3cr1tm1Litt compared with similarly treated wild-type mice
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• mice exhibit the same severity of experimental autoimmune encephalomyelitis as Cx3cr1tm1Litt homozygotes
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• following induction of experimental autoimmune encephalomyelitis, mice exhibit nonremitting spastic paralysis
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• following induction of experimental autoimmune encephalomyelitis (EAE), mice exhibit a similar reduction in NK1.1/TCRbeta- cells in the central nervous system observed in similarly treated Cx3cr1tm1Litt compared with similarly treated wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice do not exhibit the neuron loss or increase in microglial density and migration velocity observed in Cx3cr1tm1Litt/Cx3cr1+ Psen1tm1Mpm/Psen1tm1Mpm Tg(APPSwe,tauP301L)1Lfa mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• microglial density increases over time around lost neurons unlike in Cx3cr1tm1Litt/Cx3cr1tm1Litt Psen1tm1Mpm/Psen1tm1Mpm Tg(APPSwe,tauP301L)1Lfa mice
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• microglia migration velocity around lost neurons is 2-fold greater than in Cx3cr1tm1Litt heterozygotes and homozygotes
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• of YFP+ layer III neurons at 4 to 6 months
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• microglial density increases over time around lost neurons unlike in Cx3cr1tm1Litt/Cx3cr1tm1Litt Psen1tm1Mpm/Psen1tm1Mpm Tg(APPSwe,tauP301L)1Lfa mice
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• microglia migration velocity around lost neurons is 2-fold greater than in Cx3cr1tm1Litt heterozygotes and homozygotes
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• microglial density increases over time around lost neurons unlike in Cx3cr1tm1Litt/Cx3cr1tm1Litt Psen1tm1Mpm/Psen1tm1Mpm Tg(APPSwe,tauP301L)1Lfa mice
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• microglia migration velocity around lost neurons is 2-fold greater than in Cx3cr1tm1Litt heterozygotes and homozygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• S. typhimurium-infected mice exhibit a large number of bacteria in the GFP- phagocyte subset unlike in similarly treated heterozygous mice and fewer bacteria are recovered from lamina propria dendritic cells
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Retinal lesion in Ccl2tm1Rol/Ccl2tm1Rol Cx3cr1tm1Litt/Cx3cr1tm1Litt mice
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• patches of yellowish/whitish fundus lesions are seen in 17-60% of 12 month old and 30-100% of 18 month old mutants
• majority of lesions are in the temporal area (upper and lower) between the optic disc and equatorial region of the retina, with variable lesion size and lesions are rarely seen in the peripheral retinal areas
• 83-100% of mutants exposed to an approximate 800 lux light 6 hours/day for 6-7 months develop patches of yellowish and whitish lesions compared to 20-25% of wild-type mice
• aged and light-treated mutant retinas exhibit mitochondrial damage, vacuolization, and photoreceptor damage
• however, choroidal neovascularization is not seen in aged or 800 lux light treated mutants and induction of choroidal neovascularization using 532 nm diode laser does not differ from that seen in wild-type mice
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• increase in Muller glial activation
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• expression of rhodopsin, cone arrestin, and GABA are disrupted suggesting amacrine cell changes in aged mutants
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• photoreceptor inner segment damage in aged mutants
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• outer segment disorientation in aged mutants
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• expression of rhodopsin, cone arrestin, and GABA are disrupted suggesting photoreceptor degeneration
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• older mutants exhibit pigment loss in RPE cells
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• 33% of 12 month old and 50% of 18 month old mutants exhibit retinal pigment epithelium (RPE) damage, showing altered cell junction, loss of hexagonal tessellation, and uneven distribution of F-actin
• older mutants exhibit multiple vacuoles in the RPE
• all mutants exhibit RPE lesions after light-treatment (800 Lux) compared to 20% of wild-type mice
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• mice develop age- and light-mediated retinal damage
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• increase in Bruch membrane thickness in aged mutants
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• older mutants exhibit pigment loss in RPE cells
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• 33% of 12 month old and 50% of 18 month old mutants exhibit retinal pigment epithelium (RPE) damage, showing altered cell junction, loss of hexagonal tessellation, and uneven distribution of F-actin
• older mutants exhibit multiple vacuoles in the RPE
• all mutants exhibit RPE lesions after light-treatment (800 Lux) compared to 20% of wild-type mice
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• microglial cells in aged and chronic light-treated mice show shorter and larger dendrites and larger somas
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• increase in microglial activation as indicated by an increase in microglial cells in the inner plexiform layer and the outer plexiform layer at 18 months of age and in chronic-light treated mutants
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• increase in Muller glial activation
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• expression of rhodopsin, cone arrestin, and GABA are disrupted suggesting amacrine cell changes in aged mutants
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• photoreceptor inner segment damage in aged mutants
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• outer segment disorientation in aged mutants
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• expression of rhodopsin, cone arrestin, and GABA are disrupted suggesting photoreceptor degeneration
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• microglial cells in aged and chronic light-treated mice show shorter and larger dendrites and larger somas
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• bone marrow derived macrophages exhibit reduced phagocytic activity
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• increase in microglial activation as indicated by an increase in microglial cells in the inner plexiform layer and the outer plexiform layer at 18 months of age and in chronic-light treated mutants
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• microglial cells in aged and chronic light-treated mice show shorter and larger dendrites and larger somas
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• bone marrow derived macrophages exhibit reduced phagocytic activity
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• increase in microglial activation as indicated by an increase in microglial cells in the inner plexiform layer and the outer plexiform layer at 18 months of age and in chronic-light treated mutants
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| age related macular degeneration | DOID:10871 |
OMIM:PS603075 |
J:200877 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in a mouse model of thioglycollate-induced peritonitis, monocyte recruitment is reduced compared to in similarly treated wild-type mice
|
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• mice exhibit delayed onset and severity of experimental autoimmune encephalomyelitis with reduced monocyte infiltration into the central nervous system and decreased microglial cell activation compared with similarly treated wild-type mice
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• in a mouse model of thioglycollate-induced peritonitis, monocyte recruitment is reduced compared to in similarly treated wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in a mouse model of thioglycollate-induced peritonitis, monocyte recruitment is reduced compared to in similarly treated wild-type mice
|
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• mice exhibit delayed onset and severity of experimental autoimmune encephalomyelitis compared with similarly treated wild-type mice
|
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• in a mouse model of thioglycollate-induced peritonitis, monocyte recruitment is reduced compared to in similarly treated wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• decreased survival in male mice compared with Tg(SOD1*G93A)1Gur mice
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• compared with Tg(SOD1*G93A)1Gur mice
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• male mice exhibit a faster decline in hindlimb grip strength than Tg(SOD1*G93A)1Gur mice
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• male mice exhibit a faster decline in body weight than Tg(SOD1*G93A)1Gur mice
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 04/30/2024 MGI 6.23 |
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