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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Mogtm1Dpd
targeted mutation 1, Danielle Pham-Dinh
MGI:2675017
Summary 5 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Mogtm1Dpd/Mogtm1Dpd B6.129S2-Mogtm1Dpd MGI:2675026
cx2
Igh-Jtm1Aigl/Igh-J+
Mogtm1Dpd/Mogtm1Dpd
Tg(Tcra2D2,Tcrb2D2)1Kuch/0
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6 MGI:4461060
cx3
Mogtm1Dpd/Mogtm1Dpd
Tg(Tcra2D2,Tcrb2D2)1Kuch/0
involves: 129S2/SvPas * C57BL/6 MGI:4461058
cx4
Mogtm1Dpd/Mogtm1Dpd
Rag2tm1Cgn/Rag2tm1Cgn
Tg(Tcra2D2,Tcrb2D2)1Kuch/0
involves: 129S2/SvPas * C57BL/6 MGI:4461062
cx5
Mogtm1Dpd/Mogtm1Dpd
Tg(H2-Kb-Tcra,-Tcrb)1640Kurs/0
SJL.Cg-Mogtm1Dpd Tg(H2-Kb-Tcra,-Tcrb)1640Kurs MGI:5644518


Genotype
MGI:2675026
hm1
Allelic
Composition
Mogtm1Dpd/Mogtm1Dpd
Genetic
Background
B6.129S2-Mogtm1Dpd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mogtm1Dpd mutation (0 available); any Mog mutation (55 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• both homozygous mutant and wild-type mice display similar T and B cell responses against the extracellular domain of MOG, including the immunodominant MOG 35-55 T cell epitope
• no differences in secondary in vitro T cell-proliferative responses to rMOG or to an overlapping set of 31 mouse MOG peptides are observed between wild-type and homozygous mutant mice
• upon adoptive transfer, MOG-specific T cells from homozygous mutant mice and wild-type mice show an equal encephalitogenic potential, regardless of whether preactivated MOG-specific T cells or undifferentiated resting T cells are transferred
• collectively, these data imply that wild-type control mice do not develop detectable immune tolerance to MOG
• following immunization with rat rMOG (amino acids 1-125) or with the dominant MOG 35-55 encephalitogenic peptide, homozygotes display no clinical or histological CNS tissue damage, whereas all wild-type controls develop severe EAE
• following immunization with whole myelin, female homozygotes develop a less severe EAE than wild-type females, as shown by a delayed disease onset (17.9 +/- 6.6 days vs 13.4 days +/- 1.9, respectively), significantly milder clinical signs (mean maximal clinical score 1.5 +/- 1.5 vs 4.4 +/- 1.2), and a reduced mortality rate (15% vs 75%); in male homozygotes, the overall EAE severity is less than that in female homozygotes
• at day 20 after induction of EAE with whole myelin, homozygotes exhibit a reduced mean clinical score (0.5 vs 2.2), little or no CNS inflammation and no loss of myelin, whereas wild-type controls display clear signs of inflammation and some mild loss of subpial myelin (demyelination)
• at day 60 after induction of EAE with whole myelin, homozygotes display less meningeal inflammation than wild-type controls (inflammatory index 0.9 +/- 0.5 vs 2.3 +/- 1.0, respectively) and still no evidence of demyelination

nervous system
N
• at 2-, 4-, and 14 months of age, homozygotes display a normal myelin sheath architecture in the corpus callosum, striatum, cerebellum, and optic nerve relative to wild-type controls
• no differences in myelin sheath compaction, myelination kinetics or axonal structure are observed




Genotype
MGI:4461060
cx2
Allelic
Composition
Igh-Jtm1Aigl/Igh-J+
Mogtm1Dpd/Mogtm1Dpd
Tg(Tcra2D2,Tcrb2D2)1Kuch/0
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Igh-Jtm1Aigl mutation (0 available); any Igh-J mutation (14 available)
Mogtm1Dpd mutation (0 available); any Mog mutation (55 available)
Tg(Tcra2D2,Tcrb2D2)1Kuch mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• disease started between 7 and 10 weeks of age, with classical paralytic EAE signs

muscle
• in a minority of cases, with a spastic component

nervous system
• inflammatory infiltrates in the trigeminal ganglia, spinal ganglia, spinal roots despite the absence of MOG within these tissues
• inflammatory infiltrates in the peripheral nervous system despite the absence of MOG within these tissues
• lesions consisting of lymphocytic infiltration, demyelation and axonal damage in optic nerve
• lesions consisting of lymphocytic infiltration, demyelation and axonal damage in the spinal cord
• within the spinal cord and optic nerve

vision/eye
• lesions consisting of lymphocytic infiltration, demyelation and axonal damage in optic nerve

immune system
• inflammatory infiltrates in the trigeminal ganglia, spinal ganglia, spinal roots despite the absence of MOG within these tissues

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
multiple sclerosis DOID:2377 OMIM:612594
OMIM:612595
OMIM:612596
J:151335




Genotype
MGI:4461058
cx3
Allelic
Composition
Mogtm1Dpd/Mogtm1Dpd
Tg(Tcra2D2,Tcrb2D2)1Kuch/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mogtm1Dpd mutation (0 available); any Mog mutation (55 available)
Tg(Tcra2D2,Tcrb2D2)1Kuch mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• disease started between 7 and 10 weeks of age, with classical paralytic EAE signs

immune system
• between 15% and 20% of mice develop spontaneous EAE
• inflammatory infiltrates in the trigeminal ganglia, spinal ganglia, spinal roots despite the absence of MOG within these tissues

muscle
• in a minority of cases, with a spastic component

nervous system
• inflammatory infiltrates in the trigeminal ganglia, spinal ganglia, spinal roots despite the absence of MOG within these tissues
• inflammatory infiltrates in the peripheral nervous system despite the absence of MOG within these tissues
• lesions consisting of lymphocytic infiltration, demyelation and axonal damage in optic nerve
• lesions consisting of lymphocytic infiltration, demyelation and axonal damage in the spinal cord
• within the spinal cord and optic nerve

vision/eye
• lesions consisting of lymphocytic infiltration, demyelation and axonal damage in optic nerve

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
multiple sclerosis DOID:2377 OMIM:612594
OMIM:612595
OMIM:612596
J:151335




Genotype
MGI:4461062
cx4
Allelic
Composition
Mogtm1Dpd/Mogtm1Dpd
Rag2tm1Cgn/Rag2tm1Cgn
Tg(Tcra2D2,Tcrb2D2)1Kuch/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mogtm1Dpd mutation (0 available); any Mog mutation (55 available)
Rag2tm1Cgn mutation (2 available); any Rag2 mutation (99 available)
Tg(Tcra2D2,Tcrb2D2)1Kuch mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• spontaneous EAE develops in two out of six mice

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
multiple sclerosis DOID:2377 OMIM:612594
OMIM:612595
OMIM:612596
J:151335




Genotype
MGI:5644518
cx5
Allelic
Composition
Mogtm1Dpd/Mogtm1Dpd
Tg(H2-Kb-Tcra,-Tcrb)1640Kurs/0
Genetic
Background
SJL.Cg-Mogtm1Dpd Tg(H2-Kb-Tcra,-Tcrb)1640Kurs
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mogtm1Dpd mutation (0 available); any Mog mutation (55 available)
Tg(H2-Kb-Tcra,-Tcrb)1640Kurs mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• mice rarely develop spontaneous experimental autoimmune encephalomyelitis and do not develop MOG-specific antibodies





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last database update
09/27/2022
MGI 6.21
The Jackson Laboratory