Phenotypes associated with this allele

• Allele Symbol: Htt⁺
• Allele Name: wild type
• Allele ID: MGI:2176485
• Summary: 25 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
ht1	Htt^tm2Detl/Htt^+	B6J.129P2-Htt^tm2Detl	MGI:5698523
ht2	Htt^em1(IMPC)H/Htt^+	C57BL/6NTac-Htt^em1(IMPC)H/H	MGI:7414922
ht3	Htt^tm1Detl/Htt^+	involves: 129P2/OlaHsd * C57BL/6J	MGI:3573928
ht4	Htt^tm2Detl/Htt^+	involves: 129P2/OlaHsd * C57BL/6J	MGI:3583000
ht5	Htt^tm1.1Tna/Htt^+	involves: 129P2/OlaHsd * C57BL/6J	MGI:3699097
ht6	Htt^tm3Szi/Htt^+	involves: 129S1/Sv	MGI:3621448
ht7	Htt^tm1Mem/Htt^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1	MGI:3766394
ht8	Htt^tm5Mem/Htt^+	involves: 129S1/Sv * 129X1/SvJ * CD-1	MGI:3698041
ht9	Htt^tm4Mem/Htt^+	involves: 129S1/Sv * 129X1/SvJ * CD-1	MGI:3698040
ht10	Htt^tm1.1Pfs/Htt^+	involves: 129S4/SvJae * C57BL/6	MGI:3698752
ht11	Htt^tm2.1Pfs/Htt^+	involves: 129X1/SvJ * C57BL/6	MGI:3698754
ht12	Htt^tm5Detl/Htt^+	involves: C57BL/6	MGI:6400710
ht13	Htt^tm1Hay/Htt^+	involves: C57BL/6J	MGI:3586839
cx14	Fan1^em1Mem/Fan1^em1Mem Htt^tm5Mem/Htt^+ Mlh1^tm1Rak/Mlh1^tm1Rak	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6J	MGI:6489857
cx15	Htt^tm5Mem/Htt^+ Msh2^tm1Htr/Msh2^tm1Htr	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * CD-1 * FVB/N	MGI:4429638
cx16	Htt^tm1Mfc/Htt^+ Ppargc1a^tm1Dpk/Ppargc1a^+	involves: 129S1/Sv * 129X1/SvJ	MGI:3698750
cx17	Fan1^em1Mem/Fan1^em1Mem Htt^tm5Mem/Htt^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J	MGI:6489856
cx18	Htt^tm5Mem/Htt^+ Ubr5^em2Mem/Ubr5^em2Mem	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J	MGI:6489877
cx19	Htt^tm5Mem/Htt^+ Ubr5^em1Mem/Ubr5^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J	MGI:6489874
cx20	Htt^tm5Mem/Htt^+ Rrm2b^em1Mem/Rrm2b^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J	MGI:6489868
cx21	Htt^tm5Mem/Htt^+ Mtmr10^em1Mem/Mtmr10^em1Mem	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J	MGI:6489865
cx22	Fan1^em2Mem/Fan1^em2Mem Htt^tm5Mem/Htt^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J	MGI:6489862
cx23	Fan1^em2Mem/Fan1^+ Htt^tm3Mem/Htt^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J	MGI:6489859
cx24	Fan1^em2Mem/Fan1^em2Mem Htt^tm3Mem/Htt^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J	MGI:6489858
cx25	Htt^tm1Hay/Htt^+ Tg(YAC72)2511Hay/0	involves: FVB/N	MGI:5298846

Genotype
MGI:5698523

ht1

• Allelic Composition: Htt^tm2Detl/Htt⁺
• Genetic Background: B6J.129P2-Htt^tm2Detl

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

nervous system

microgliosis ( J:220868 )

♂ • mice with about 250 CAG repeats exhibit increased proliferation of microglia in the striatum

decreased oligodendrocyte number ( J:220868 )

♂ • mice with about 250 CAG repeats have decreased numbers of mature oligodendrocytes in the brain at P14

abnormal oligodendrocyte physiology ( J:220868 )

♂ • mice with about 250 CAG repeats exhibit enhanced proliferation of oligodendrocyte precursor cells in the corpus callosum and striatum at 9 and 12 months of age

♂ • however, the number of oligodendrocyte precursor cells is normal

♂ • primary oligodendrocyte precursor cells from P6 mice with about 250 CAG repeats exhibit an extended S-phase

abnormal striatum morphology ( J:220868 )

♂ • mice with about 250 CAG repeats show a reduction in the striatum volume by 6 months of age but not at 3 months

♂ • striatal metabolites are altered by 9 months of age in mice with about 250 CAG repeats, with lower levels of N-acetylaspartate at 9 months, and lower levels of gamma-aminobutyric acid (GABA), glutamate, NAA, creatine + PCr and increased levels of glutamine and taurine at 12 months of age

decreased neocortex volume ( J:220868 )

♂ • mice with about 250 CAG repeats show a reduction in the neocortex volume by 6 months of age but not at 3 months

brain atrophy ( J:220868 )

♂ • mice backcrossed to C57BL/6J for 8 generations yields mice with about 250 CAG repeats which show acceleration of brain atrophy (striatum and neocortex) compared to mice with 150 or 200 CAG repeats that is most robust between 2 and 6 months of age

decreased myelin sheath thickness ( J:220868 )

♂ • mice with about 250 CAG repeats exhibit numerous smaller axons that are hypomyelinated with increased G-ratios (diameter of axon/outer diameter of the myelinaged fiber) in the corpus callosum at 12 months of age, indicating thinner myelin sheaths

neuronal intranuclear inclusions ( J:220868 )

♂ • mice with about 250 CAG repeats show nuclear progressive accumulation of mutant HTT aggregates from 6 to 12 months of age

abnormal myelination ( J:220868 )

♂ • mice with about 250 CAG repeats show developmental delay of myelination, with lower levels of all isoforms of myelin basic protein and myelin oligodendrocyte glycoprotein in the striatum at P14

dysmyelination ( J:220868 )

♂ • mice with about 250 CAG repeats show fewer myelinated axons in the corpus callosum at P14

growth/size/body

weight loss ( J:220868 )

♂ • mice with about 250 CAG repeats exhibit lower body weight; they gain body weight normally up to 4 months, stop gaining weight and then lose weight

behavior/neurological

impaired coordination ( J:220868 )

♂ • mice with about 250 CAG repeats exhibit a motor deficit on the balance beam at 6 months of age, spending more time to cross the beam; motor deficits progress with age

hematopoietic system

microgliosis ( J:220868 )

♂ • mice with about 250 CAG repeats exhibit increased proliferation of microglia in the striatum

immune system

microgliosis ( J:220868 )

♂ • mice with about 250 CAG repeats exhibit increased proliferation of microglia in the striatum

homeostasis/metabolism

increased taurine level ( J:220868 )

♂ • mice with about 250 CAG repeats show increased levels of taurine in the striatum at 12 months of age

cellular

microgliosis ( J:220868 )

♂ • mice with about 250 CAG repeats exhibit increased proliferation of microglia in the striatum

decreased oligodendrocyte number ( J:220868 )

♂ • mice with about 250 CAG repeats have decreased numbers of mature oligodendrocytes in the brain at P14

abnormal oligodendrocyte physiology ( J:220868 )

♂ • mice with about 250 CAG repeats exhibit enhanced proliferation of oligodendrocyte precursor cells in the corpus callosum and striatum at 9 and 12 months of age

♂ • however, the number of oligodendrocyte precursor cells is normal

♂ • primary oligodendrocyte precursor cells from P6 mice with about 250 CAG repeats exhibit an extended S-phase

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Huntington's disease		DOID:12858	OMIM:143100	J:220868

Genotype
MGI:7414922

ht2

• Allelic Composition: Htt^em1(IMPC)H/Htt⁺
• Genetic Background: C57BL/6NTac-Htt^em1(IMPC)H/H

Data Sources

IMPC Data for Htt

behavior/neurological

increased grip strength ( J:211773 )

♀

IMPC - HAR

Genotype
MGI:3573928

ht3

• Allelic Composition: Htt^tm1Detl/Htt⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

behavior/neurological

behavior/neurological phenotype ( J:67074 )

N • during tail suspension, a similar % (<20%) of wild-type and heterozygous mutant mice tend to clasp

impaired limb coordination ( J:67074 )

• at >40 weeks of age, heterozygotes show a late-onset increase in the average distance between front and hind paws ('overlap' distance) relative to wild-type mice

decreased locomotor activity ( J:67074 )

• heterozygotes are viable, fertile and developmentally normal; however, 1 out of 10 heterozygotes remains inactive upon removal of the cage lid whereas all wild-type mice show exploratory activity by walking around the cage

growth/size/body

decreased body size ( J:67074 )

• at 34 weeks of age, some heterozygotes exhibit an extreme size reduction relative to wild-type mice

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:67074 )

N • heterozygotes display normal blood glucose levels relative to wild-type mice

nervous system

nervous system phenotype ( J:67074 )

N • heterozygotes display no extreme reductions in major brain regions up to 90 weeks of age

N • no reactive gliosis or formation of neuronal intranuclear inclusions is observed

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Huntington's disease		DOID:12858	OMIM:143100	J:67074

Genotype
MGI:3583000

ht4

• Allelic Composition: Htt^tm2Detl/Htt⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

mortality/aging

premature death ( J:67074 )

• only 3 of 45 heterozygotes die prior to 1 year of age; heterozygotes typically survive for >1 year

behavior/neurological

abnormal behavior ( J:123681 )

• the discrepancy between onset age of behavioral and neurological phenotypes is believed to reflect the percentage of C57BL/6 in the strain background (50-75% C57BL/6 - early onset (J:67074), 75-90% C57BL/6 - late onset (J:123681))

abnormal motor capabilities/coordination/movement ( J:67074 )

• heterozygotes are viable and developmentally normal but present symptoms of motor deficits with an onset of ~60 weeks; symptom presentation is variable among individual mutants

limb grasping ( J:67074 )

• during tail suspension, >60% of old heterozygotes (>40 weeks) versus only <20% of wild-type or Hdh^tm1Detl homozygotes (carrying a 80 unit CAG repeat) tend to clasp

• the tendency to clasp is a late-onset trait conferred by the Hdh^tm2Detl allele

abnormal motor coordination/balance ( J:67074 )

• at 5.0 rpm., heterozygotes (15-40 weeks) stay for a significantly shorter time on a slowly rotating rod relative to age-matched wild-type mice

enhanced coordination ( J:123681 )

• at 20 weeks of age mice performed better in motor performance on the accelerated rotarod than wild-type controls

• heterozygotes outperform homozygotes on the rotarod up to 40 weeks of age

impaired balance ( J:123681 )

• beginning at 70 weeks of age time to traverse 11 mm round and 5 mm square balance beam is increased as compared to wild-type

• 50% of 100 week old mice fail to traverse the 5 mm beam

• 63% of 100 week old mice exhibit a hindlimb drag while traversing beam

impaired limb coordination ( J:67074 )

• at >40 weeks of age, heterozygotes show a late-onset increase in the average distance between front and hind paws ('overlap' distance) relative to age-matched wild-type mice or Hdh^tm1Detl heterozygotes (carrying a 80 unit CAG repeat)

abnormal gait ( J:67074 , J:123681 )

• old heterozygotes (greater than 40 weeks) exhibit an abnormal gait relative to wild-type mice (J:67074)

• old (but not young) heterozygotes display a 2-fold increase in stride and base length variation relative to wild-type mice, suggesting that the mutation causes a late-onset variability in gait (J:67074)

• staggering gait observed in animals at 100 weeks of age (J:123681)

short stride length ( J:123681 )

• hindpaw and forepaw stride lengths are reduced in heterozygotes at 100 weeks of age as compared to wild-type

decreased locomotor activity ( J:67074 )

• at 15-40 weeks of age, a few heterozygotes remain inactive upon removal of the cage lid whereas all wild-type mice show exploratory activity by walking around the cage

• the proportion of heterozygotes tending to remain inactive increases significantly with age (>40 weeks), indicating that the tendency to be inactive is a late-onset trait conferred by the mutant allele

nervous system

nervous system phenotype ( J:67074 )

N • heterozygotes display no extreme reductions in major brain regions up to 52 weeks of age

gliosis ( J:67074 )

• mutant mice exhibit significant reactive gliosis in the striatum; notably, neuronal number remains relatively unaffected

abnormal dorsal striatum morphology ( J:123681 )

• striatal dopamine D1 receptor sites are decreased by 42% as compared to wild-type at 100 weeks of age

• striatal dopamine D2 receptor sites are decreased by 17% as compared to wild-type at 100 weeks of age

abnormal ventral striatum morphology ( J:123681 )

• striatal dopamine D1 receptor sites are decreased by 50% as compared to wild-type at 100 weeks of ag

• striatal dopamine D2 receptor sites are decreased by 17% as compared to wild-type at 100 weeks of age

neuron degeneration ( J:67074 )

• starting at ~40 weeks, mutants exhibit neuronal intranuclear inclusions (NIIs) predominantly in the striatum; however, no dystrophic neurites are observed

growth/size/body

decreased body size ( J:67074 )

• at 52 weeks of age, some heterozygotes are significantly smaller than wild-type littermates

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:67074 )

N • heterozygotes display normal blood glucose levels relative to wild-type mice

cellular

gliosis ( J:67074 )

• mutant mice exhibit significant reactive gliosis in the striatum; notably, neuronal number remains relatively unaffected

Genotype
MGI:3699097

ht5

• Allelic Composition: Htt^tm1.1Tna/Htt⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

nervous system

astrocytosis ( J:76017 )

• exhibit an increase in glial fibrillary acidic protein (GFAP)-positive cells in the substantia nigra and the globus pallidus at 40 weeks of age, indicating astrocytosis

cellular

astrocytosis ( J:76017 )

• exhibit an increase in glial fibrillary acidic protein (GFAP)-positive cells in the substantia nigra and the globus pallidus at 40 weeks of age, indicating astrocytosis

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Huntington's disease		DOID:12858	OMIM:143100	J:76017

Genotype
MGI:3621448

ht6

• Allelic Composition: Htt^tm3Szi/Htt⁺
• Genetic Background: involves: 129S1/Sv

behavior/neurological

increased exploration in new environment ( J:106763 )

• excessive numbers of errors in a Barnes circular maze in early trials, due to increased exploration

Genotype
MGI:3766394

ht7

• Allelic Composition: Htt^tm1Mem/Htt⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1

normal phenotype

no abnormal phenotype detected ( J:27183 )

• animals are normal is size and appearance, with no obvious behavioral or morphological abnormalities

Genotype
MGI:3698041

ht8

• Allelic Composition: Htt^tm5Mem/Htt⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * CD-1

nervous system

abnormal striatum morphology ( J:60937 )

abnormal medium spiny neuron morphology ( J:60937 )

• exhibit relocation of the mutant protein to the nucleus in medium sized spiny neurons and much later, the formation of morphologic nuclear inclusions and insoluble aggregate that are hallmarks of Huntington's Disease in humans, although at a slower rate than in homozygotes

neuronal intranuclear inclusions ( J:60937 )

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Huntington's disease		DOID:12858	OMIM:143100	J:60937

Genotype
MGI:3698040

ht9

• Allelic Composition: Htt^tm4Mem/Htt⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * CD-1

nervous system

abnormal striatum morphology ( J:60937 )

abnormal medium spiny neuron morphology ( J:60937 )

• exhibit relocation of the mutant protein to the nucleus in medium sized spiny neurons and much later, the formation of morphologic nuclear inclusions and insoluble aggregate that are hallmarks of Huntington's Disease in humans, although at a slower rate than seen in homozygotes

neuronal intranuclear inclusions ( J:60937 )

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Huntington's disease		DOID:12858	OMIM:143100	J:60937

Genotype
MGI:3698752

ht10

• Allelic Composition: Htt^tm1.1Pfs/Htt⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

behavior/neurological

increased aggression towards mice ( J:54906 )

• exhibit heightened aggression amongst group housed males and females and increased incidence of isolation-induced aggression in the resident-intruder test

nervous system

decreased brain size ( J:54906 )

• brains are, on average, 10-15% smaller at 4-6 months of age

• however, do not exhibit any pathological gliosis, ventricular enlargement, or neurodegeneration at 4-6 and 16-17 months of age

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Huntington's disease		DOID:12858	OMIM:143100	J:54906

Genotype
MGI:3698754

ht11

• Allelic Composition: Htt^tm2.1Pfs/Htt⁺
• Genetic Background: involves: 129X1/SvJ * C57BL/6

behavior/neurological

increased aggression towards mice ( J:54906 )

• exhibit heightened aggression amongst group housed males and females and increased incidence of isolation-induced aggression in the resident-intruder test

nervous system

decreased brain size ( J:54906 )

• brains are, on average, 10-15% smaller at 4-6 months of age

• however, do not exhibit any pathological gliosis, ventricular enlargement, or neurodegeneration at 4-6 and 16-17 months of age

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Huntington's disease		DOID:12858	OMIM:143100	J:54906

Genotype
MGI:6400710

ht12

• Allelic Composition: Htt^tm5Detl/Htt⁺
• Genetic Background: involves: C57BL/6

behavior/neurological

behavior/neurological phenotype ( J:250587 )

N • mice do not exhibit signs of tremor, hunching, unsteady movements or staggering gait up to 70 weeks of age and do not exhibit spontaneous or handling-induced seizures

abnormal motor learning ( J:250587 )

♂ • males, but not females, exhibit enhanced fast motor learning (performance on the rotarod across all 3 testing days) at 40 and 60 weeks of age

increased thigmotaxis ( J:250587 )

♀ • females, but not males, spend increased time along the walls of the test chamber, indicating increased thigmotaxis and possible anxiety

impaired coordination ( J:250587 )

♂ • at 60 weeks of age, males, but not females, show a reduction in motor coordination on the 2nd and 3rd days of testing on the accelerating rotarod, with a shorter latency to fal

decreased grip strength ( J:250587 )

• males and females exhibit reduced grip strength, with a significant decrease in females at 50 weeks of age

hunched posture ( J:250587 )

♀ • females spend more time with their bodies contracted, or hunched, at nearly all ages

abnormal gait ( J:250587 )

• females, but not males, show a reduction in hind paw step cycle

• males, but not females, show a reduction in front paw base of support at 60 weeks of age, indicating reduced stability

long stride length ( J:250587 )

♂ • males, but not females, show an increase in front paw stride length

decreased locomotor activity ( J:250587 )

• mice exhibit an overall decrease in spontaneous locomotion during the active dark phase, with females being more severely affected than males at 70 weeks of age

• however, no differences in spontaneous activity during the light phase are seen

growth/size/body

weight loss ( J:250587 )

• mice show reduced weight by 70 weeks of age

• males exhibit a 9.4% reduced body weight by 40 weeks of age while females exhibit a 9.4% reduced body weight by 30 weeks of age

mortality/aging

prenatal lethality, incomplete penetrance ( J:250587 )

• fewer than the expected number of pups are seen, indicating reduced viability

nervous system

abnormal striatum morphology ( J:250587 )

• females, but not males, show a reduction in striatal DARPP-32 (a neuropathological maker of Huntingtons Disease pathogenesis) expression with no cell loss

• however, no differences in synaptophysin or CB1 receptor expression in the striatum are seen

• Htt aggregates are seen in the striatum, at similar levels in males and females

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Huntington's disease		DOID:12858	OMIM:143100	J:250587

Genotype
MGI:3586839

ht13

• Allelic Composition: Htt^tm1Hay/Htt⁺
• Genetic Background: involves: C57BL/6J

behavior/neurological

abnormal learning/memory/conditioning ( J:25941 )

• significantly slower to find the hidden platform when it was moved to a new location in the reverse trial of the Morris water maze test, indicating cognitive defects associated with acquiring or using new information in the face of exisiting information

hyperactivity ( J:25941 )

• significantly more active throughout both light- and dark-phases when placed in a novel photocell cage than controls

hyperresponsive ( J:25941 )

• more reactive to handling than controls

nervous system

abnormal globus pallidus morphology ( J:25941 )

• fewer neurons in the globus pallidus, however the caudate/putamen, cerebral cortex, and corpus callosum were normal

abnormal subthalamic nucleus morphology ( J:25941 )

• subthalamic nucleus is decreased in size and volume and contains fewer neurons

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Huntington's disease		DOID:12858	OMIM:143100	J:25941

Genotype
MGI:6489857

cx14

• Allelic Composition: Fan1^em1Mem/Fan1^em1Mem; Htt^tm5Mem/Htt⁺; Mlh1^tm1Rak/Mlh1^tm1Rak
• Genetic Background: involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6J

cellular

cellular phenotype ( J:298297 )

N • Htt CAG repeat stability is normal

Genotype
MGI:4429638

cx15

• Allelic Composition: Htt^tm5Mem/Htt⁺; Msh2^tm1Htr/Msh2^tm1Htr
• Genetic Background: involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * CD-1 * FVB/N

nervous system

neuronal intranuclear inclusions ( J:81666 )

• intranuclear accumulation of mutant huntingtin is delayed 5 months compared to in Htt^tm5Mem heterozygotes

Genotype
MGI:3698750

cx16

• Allelic Composition: Htt^tm1Mfc/Htt⁺; Ppargc1a^tm1Dpk/Ppargc1a⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

behavior/neurological

impaired coordination ( J:116058 )

• rotarod performance is severely impaired and much worse than in mice carrying the Hdh^tm1Mfc knock-in allele

nervous system

abnormal striatum morphology ( J:116058 )

• striatal neuronal volumes are significantly decreased in 6-month old mutants compared to mice carrying the Hdh^tm1Mfc knock-in allele

neuron degeneration ( J:116058 )

• early neuronal degeneration appears in the striatum and the medial septal nucleus by 3 months of age

• mutants exhibit increased susceptibility to 3-nitropropionic acid, developing larger striatal lesions and increased number of degenerating neurons compared to mice carrying the Hdh^tm1Mfc knock-in allele

Genotype
MGI:6489856

cx17

• Allelic Composition: Fan1^em1Mem/Fan1^em1Mem; Htt^tm5Mem/Htt⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6J

cellular

abnormal cell physiology ( J:298297 )

• expansion of the Htt CAG triplet repeats in striatum and liver at 5 months of age

increased cellular sensitivity to alkylating agents ( J:298297 )

• in response to mitomycin C in embryonic fibroblasts

Genotype
MGI:6489877

cx18

• Allelic Composition: Htt^tm5Mem/Htt⁺; Ubr5^em2Mem/Ubr5^em2Mem
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6J

cellular

abnormal cell physiology ( J:298297 )

• expansion of the Htt CAG triplet repeats in striatum and liver at 5 months of age

Genotype
MGI:6489874

cx19

• Allelic Composition: Htt^tm5Mem/Htt⁺; Ubr5^em1Mem/Ubr5⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6J

cellular

abnormal cell physiology ( J:298297 )

• expansion of the Htt CAG triplet repeats in striatum and liver at 5 months of age

Genotype
MGI:6489868

cx20

• Allelic Composition: Htt^tm5Mem/Htt⁺; Rrm2b^em1Mem/Rrm2b⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6J

cellular

cellular phenotype ( J:298297 )

N • Htt CAG repeat stability is normal

Genotype
MGI:6489865

cx21

• Allelic Composition: Htt^tm5Mem/Htt⁺; Mtmr10^em1Mem/Mtmr10^em1Mem
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6J

cellular

abnormal cell physiology ( J:298297 )

• expansion of the Htt CAG triplet repeats in striatum and liver at 5 months of age

Genotype
MGI:6489862

cx22

• Allelic Composition: Fan1^em2Mem/Fan1^em2Mem; Htt^tm5Mem/Htt⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6J

cellular

abnormal cell physiology ( J:298297 )

• expansion of the Htt CAG triplet repeats in striatum and liver at 5 months of age

Genotype
MGI:6489859

cx23

• Allelic Composition: Fan1^em2Mem/Fan1⁺; Htt^tm3Mem/Htt⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6J

cellular

abnormal cell physiology ( J:298297 )

• expansion of the Htt CAG triplet repeats in striatum and liver at 8 months of age

Genotype
MGI:6489858

cx24

• Allelic Composition: Fan1^em2Mem/Fan1^em2Mem; Htt^tm3Mem/Htt⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6J

cellular

abnormal cell physiology ( J:298297 )

• some expansion of the Htt CAG triplet repeats in striatum and liver at 8 months of age

Genotype
MGI:5298846

cx25

• Allelic Composition: Htt^tm1Hay/Htt⁺; Tg(YAC72)2511Hay/0
• Genetic Background: involves: FVB/N

reproductive system

testicular atrophy ( J:67366 )

♂ • in some mice

endocrine/exocrine glands

testicular atrophy ( J:67366 )

♂ • in some mice