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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Acetm1Keb
targeted mutation 1, Kenneth E Bernstein
MGI:2155954
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Acetm1Keb/Acetm1Keb involves: 129S1/Sv * 129X1/SvJ MGI:4830256
hm2
Acetm1Keb/Acetm1Keb involves: 129S1/Sv * 129X1/SvJ * C57BL/6J MGI:3618293
ht3
Acetm1Keb/Ace+ involves: 129S1/Sv * 129X1/SvJ * C57BL/6J MGI:3618294
ht4
Acetm1Keb/Acetm5Keb involves: 129S1/Sv * 129X1/SvJ MGI:3042132


Genotype
MGI:4830256
hm1
Allelic
Composition
Acetm1Keb/Acetm1Keb
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Acetm1Keb mutation (0 available); any Ace mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• blood pressure is unaffected by angiotensin I infusion unlike in wild-type mice

cardiovascular system
• blood pressure is unaffected by angiotensin I infusion unlike in wild-type mice




Genotype
MGI:3618293
hm2
Allelic
Composition
Acetm1Keb/Acetm1Keb
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Acetm1Keb mutation (0 available); any Ace mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• contrary to previous findings (J:25284), homozygotes generated from F1 intercrosses are obtained at the expected Mendelian frequency

cardiovascular system
• homozygotes exhibit thickened intrarenal arteries and arterioles as a result of medial hyperplasia
• thickened and hyperplastic renal arteries are observed
• inflammatory cells can be seen around the renal arteries with some infiltration into the vessel wall
• homozygotes exhibit an increase in average pulse rates (676 12 beats/min) relative to wild-type (626 16 beats/min) or heterozygous mutant mice (625 8 beats/min)
• homozygotes exhibit a significantly reduced average systolic blood pressure (73.3 1.7 mm Hg) relative to wild-type (110.1 1.9 mm Hg) or heterozygous mutant mice (107.3 1.6 mm Hg)

renal/urinary system
• homozygotes exhibit thickened intrarenal arteries and arterioles as a result of medial hyperplasia
• thickened and hyperplastic renal arteries are observed
• inflammatory cells can be seen around the renal arteries with some infiltration into the vessel wall
• following water deprivation, homozygotes display a reduction in electrolyte concentration, with a significantly lower urinary sodium to potassium ratio
• following water deprivation, homozygotes produce ~50% of the total aldosterone levels found in the urine of wild-type mice
• following water deprivation, homozygotes exhibit increased potassium excretion relative to wild-type mice
• when water is freely accessible, homozygotes exhibit a slightly lower average urine osmolarity (770 30 mOSM/kg ) relative to wild-type mice (1070 60 mOSM/kg)
• following water deprivation, homozygotes produce a higher (2x) volume of urine that is <50% as concentrated (1300 10 mOSM/kg) than that of wild-type mice (3000 300 mOSM/kg)
• regions of inflammatory infiltrate are seen at the cortical medullary junction
• regions of inflammatory infiltrate are seen at the cortical medullary junction
• mutant kidneys display papillary atresia
• mutant kidneys display renal papillary atrophy
• mutant kidneys display a thinned medulla
• mutant kidneys display dilated renal calyses
• homozygotes display dilation of the renal pelvis and calyces
• homozygous mutant kidneys are ~75% of the mass of wild-type kidneys
• when water is freely accessible, homozygotes show a 2-fold increase in urinary output relative to wild-type mice

reproductive system
• male homozygotes sire significantly smaller litters than wild-type males (3.3 1.4 vs 9.7 1.5 pups per litter, respectively)
• male homozygotes display reduced fertility, despite normal testis histology and normal sperm number, morphology, and motility
• in contrast, female homozygotes are fertile and produce normal litter sizes

homeostasis/metabolism
• homozygotes display significantly increased plasma creatinine levels (0.56 0.06 mg/dl) relative to wild-type mice (0.30 0.04 mg/dl)
• following water deprivation, homozygotes display a reduction in electrolyte concentration, with a significantly lower urinary sodium to potassium ratio
• following water deprivation, homozygotes produce ~50% of the total aldosterone levels found in the urine of wild-type mice
• following water deprivation, homozygotes exhibit increased potassium excretion relative to wild-type mice
• when water is freely accessible, homozygotes exhibit a slightly lower average urine osmolarity (770 30 mOSM/kg ) relative to wild-type mice (1070 60 mOSM/kg)
• following water deprivation, homozygotes produce a higher (2x) volume of urine that is <50% as concentrated (1300 10 mOSM/kg) than that of wild-type mice (3000 300 mOSM/kg)

immune system
• regions of inflammatory infiltrate are seen at the cortical medullary junction




Genotype
MGI:3618294
ht3
Allelic
Composition
Acetm1Keb/Ace+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Acetm1Keb mutation (0 available); any Ace mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• unexpectedly, heterozygous males display no significant differences in systolic blood pressure (110.2 2.4 mm Hg) relative to wild-type males (109.9 2.3 mm Hg)




Genotype
MGI:3042132
ht4
Allelic
Composition
Acetm1Keb/Acetm5Keb
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Acetm1Keb mutation (0 available); any Ace mutation (15 available)
Acetm5Keb mutation (0 available); any Ace mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• plasma renin levels are elevated although less than in mice homozygous for Acetm1Keb
• conversion of angiotensin I into angiotensin II is reduced compared to wildtype mice and mice homozygous for Acetm5Keb





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last database update
04/19/2016
MGI 6.03
The Jackson Laboratory