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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Clutm1Jakh
targeted mutation 1, Judith A K Harmony
MGI:2181011
Summary 5 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Clutm1Jakh/Clutm1Jakh involves: 129S2/SvPas MGI:3784304
hm2
Clutm1Jakh/Clutm1Jakh involves: 129S2/SvPas * Black Swiss MGI:5432925
hm3
Clutm1Jakh/Clutm1Jakh involves: Black Swiss * FVB/N MGI:2663412
cx4
Apoetm1Unc/Apoetm1Unc
Clutm1Jakh/Clutm1Jakh
Tg(APPV717F)109Ili/Tg(APPV717F)109Ili
involves: 129P2/OlaHsd * 129S2/SvPas MGI:3721541
cx5
Clutm1Jakh/Clutm1Jakh
Tg(APPV717F)109Ili/Tg(APPV717F)109Ili
involves: 129S2/SvPas MGI:3721530


Genotype
MGI:3784304
hm1
Allelic
Composition
Clutm1Jakh/Clutm1Jakh
Genetic
Background
involves: 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Clutm1Jakh mutation (1 available); any Clu mutation (13 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• astrocytes secrete a normal composition of lipid particles




Genotype
MGI:5432925
hm2
Allelic
Composition
Clutm1Jakh/Clutm1Jakh
Genetic
Background
involves: 129S2/SvPas * Black Swiss
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Clutm1Jakh mutation (1 available); any Clu mutation (13 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
N
• mice exhibit no evidence of tubulointerstitial disease, vascular lesions, inflammatory infiltrates, necrosis, or amyloid deposits, regardless of the extent of glomerulopathy
• glomerular basement membranes are normal and lack discernible deposits
• collapse of capillary lumens at 21 months of age
• an occasional mutant develops hematuria
• up to 75% of glomeruli exhibit moderate to severe mesangial lesions at 21 months of age
• mesangial hypercellularity noted in 6-mo-old mice that have undergone unilateral nephrectomy at 3 months and are then fed a high-protein diet
• electron-dense tubulo-fibrillar structures arranged in parallel arrays are detected in the mesangial matrix at 21 months, consistent with immune complex deposits
• more electron-dense deposits found in 6-mo-old mice that have undergone unilateral nephrectomy at 3 months and are then fed a high-protein diet
• variable mesangial expansion observed at 21 months, but not at 6 months, of age
• more severe mesangial expansion noted in 6-mo-old mice that have undergone unilateral nephrectomy at 3 months and are then fed a high-protein diet
• at 21 months of age, mice display progressive mesangial expansion, collapse of capillary lumens, and deposition of collagen and immune complexes, unlike wild-type and heterozygous controls
• immune complexes of IgG, IgM, IgA, and in some cases C1q, C3, and C9 are detected in the mesangium at 21 months of age
• immune complexes of IgG, IgM and IgA are noted as early as 4 weeks of age
• increased deposition of C1q and C3 in 6-mo-old mice that have undergone unilateral nephrectomy at 3 months and are then fed a high-protein diet
• accumulation of collagen deposits in the glomeruli

homeostasis/metabolism
N
• mice display no signs of proteinuria or any alterations in serum and urine proteins relative to controls
• an occasional mutant develops hematuria

cardiovascular system
• collapse of capillary lumens at 21 months of age




Genotype
MGI:2663412
hm3
Allelic
Composition
Clutm1Jakh/Clutm1Jakh
Genetic
Background
involves: Black Swiss * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Clutm1Jakh mutation (1 available); any Clu mutation (13 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• after immunization with cardiac myosin, mutant hearts become pale and enlarged, mutants exhibit 3-fold greater heart tissue injury than wild-type
• 21 days after myocarditis initiation, mice show significant cardiac tissue injury than wild-type mice
• after immunization, myocyte necrosis is observed in some animals
• 7 weeks following myocarditis, widespread loss of myocardial fibers is found in mutant hearts, whereas none is seen in wild-type controls
• ventricular damage in females is 6-fold greater than in wild-type females; males do not show as severe cardiac damage
• postmyocarditis heart function is impaired with decreased shortening fraction measured in mutants;
• severe, diffuse inflammation with large inflammatory aggregates occurs after immunization with cardiac myosin
• severe myocarditis after immunization with cardiac myosin, more severe than in wild-type

muscle
• after immunization, myocyte necrosis is observed in some animals
• 7 weeks following myocarditis, widespread loss of myocardial fibers is found in mutant hearts, whereas none is seen in wild-type controls
• postmyocarditis heart function is impaired with decreased shortening fraction measured in mutants;

immune system
• severe, diffuse inflammation with large inflammatory aggregates occurs after immunization with cardiac myosin
• severe myocarditis after immunization with cardiac myosin, more severe than in wild-type

homeostasis/metabolism
• immunized mice show cardiac edema




Genotype
MGI:3721541
cx4
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Clutm1Jakh/Clutm1Jakh
Tg(APPV717F)109Ili/Tg(APPV717F)109Ili
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (68 available)
Clutm1Jakh mutation (1 available); any Clu mutation (13 available)
Tg(APPV717F)109Ili mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• at 6 months of age, most mice have substantial amyloid beta (Abeta) deposits
• by 12 months of age, mice have more amyloid beta (Abeta) deposits in the hippocampus and cortex than other genotypes
• Abeta deposits are more numerous and fill all parts of hippocampus and some of the cortex by 12 months; abundant compact and diffuse plaques are observed
• mice have greater levels of thioflavine-S-positive (fibrillar) Abeta deposits than other genotypes, similar to transgenic homozygotes with normal Apoe and Clu
• at 3 months, cerebral spinal fluid levels of Abeta40 and Abeta42 are elevated

homeostasis/metabolism
• mice have significant amyloid burden, greater than shown by other genotypes
• at 12 months, mice have highest tissue levels of soluble Abeta40 and Abeta42, with high levels of insoluble Abeta42
• at 3 months, mice have higher levels of carbonate soluble Abeta40 and Abeta42 compared to other genotypes
• at 6 months of age, most mice have substantial amyloid beta (Abeta) deposits
• by 12 months of age, mice have more amyloid beta (Abeta) deposits in the hippocampus and cortex than other genotypes
• Abeta deposits are more numerous and fill all parts of hippocampus and some of the cortex by 12 months; abundant compact and diffuse plaques are observed
• mice have greater levels of thioflavine-S-positive (fibrillar) Abeta deposits than other genotypes, similar to transgenic homozygotes with normal Apoe and Clu
• at 3 months, cerebral spinal fluid levels of Abeta40 and Abeta42 are elevated

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:107702




Genotype
MGI:3721530
cx5
Allelic
Composition
Clutm1Jakh/Clutm1Jakh
Tg(APPV717F)109Ili/Tg(APPV717F)109Ili
Genetic
Background
involves: 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Clutm1Jakh mutation (1 available); any Clu mutation (13 available)
Tg(APPV717F)109Ili mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• by 12 months of age, ~60% of mice show amyloid beta (Abeta) deposition (J:78357)
• decreased percentage of Abeta-immunoreactive deposits that are thioflavine-S-positive (2.46 vs 19.4% thioflavine load/Abeta load) compared to Clu-sufficient mice (J:78357)
• many Abeta deposits have few or no detectable dystrophic neurites around them (J:78357)
• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex (J:107702)
• a 10-fold reduction in dystrophic neurites in hippocampi at 12 months compared to Clu-sufficient transgenic mice and a 5-fold reduction in number of dystrophic neurites per amyloid deposit

homeostasis/metabolism
• only 20% of mice have thioflavine-S-positive (fibrillar Abeta or amyloid) deposits in the cortex at 12 months
• mice have lower hippocampal amyloid burden (0.89%) at 12 months than Clu-sufficient transgenic mice; amyloid load increases to 2.25% by 15 months
• by 12 months of age, ~60% of mice show amyloid beta (Abeta) deposition (J:78357)
• decreased percentage of Abeta-immunoreactive deposits that are thioflavine-S-positive (2.46 vs 19.4% thioflavine load/Abeta load) compared to Clu-sufficient mice (J:78357)
• many Abeta deposits have few or no detectable dystrophic neurites around them (J:78357)
• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex (J:107702)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:78357





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last database update
04/26/2016
MGI 6.03
The Jackson Laboratory