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Phenotypes Associated with This Genotype
Genotype
MGI:5527432
Allelic
Composition
Ccl2tm1Rol/Ccl2tm1Rol
Cx3cr1tm1Litt/Cx3cr1tm1Litt
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ccl2tm1Rol mutation (2 available); any Ccl2 mutation (8 available)
Cx3cr1tm1Litt mutation (6 available); any Cx3cr1 mutation (29 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Retinal lesion in Ccl2tm1Rol/Ccl2tm1Rol Cx3cr1tm1Litt/Cx3cr1tm1Litt mice

vision/eye
• 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
• increase in Muller glial activation
• expression of rhodopsin, cone arrestin, and GABA are disrupted suggesting amacrine cell changes in aged mutants
• photoreceptor inner segment damage in aged mutants
• outer segment disorientation in aged mutants
• expression of rhodopsin, cone arrestin, and GABA are disrupted suggesting photoreceptor degeneration
• older mutants exhibit pigment loss in RPE cells
• 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
• mice develop age- and light-mediated retinal damage
• increase in Bruch membrane thickness in aged mutants

pigmentation
• older mutants exhibit pigment loss in RPE cells
• 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

nervous system
• microglial cells in aged and chronic light-treated mice show shorter and larger dendrites and larger somas
• 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
• increase in Muller glial activation
• expression of rhodopsin, cone arrestin, and GABA are disrupted suggesting amacrine cell changes in aged mutants
• photoreceptor inner segment damage in aged mutants
• outer segment disorientation in aged mutants
• expression of rhodopsin, cone arrestin, and GABA are disrupted suggesting photoreceptor degeneration

hematopoietic system
• microglial cells in aged and chronic light-treated mice show shorter and larger dendrites and larger somas
• bone marrow derived macrophages exhibit reduced phagocytic activity
• 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

immune system
• microglial cells in aged and chronic light-treated mice show shorter and larger dendrites and larger somas
• bone marrow derived macrophages exhibit reduced phagocytic activity
• 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

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
age related macular degeneration DOID:10871 OMIM:PS603075
J:200877


Contributing Projects:
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
02/23/2021
MGI 6.16
The Jackson Laboratory