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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Adora2atm1Jfc
targeted mutation 1, Jiang-Fan Chen
MGI:2155985
Summary 6 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Adora2atm1Jfc/Adora2atm1Jfc B6.129S4-Adora2atm1Jfc MGI:5473699
hm2
Adora2atm1Jfc/Adora2atm1Jfc involves: 129 * C57BL/6 MGI:3625471
hm3
Adora2atm1Jfc/Adora2atm1Jfc involves: 129S4/SvJae * 129S6/SvEvTac MGI:3622795
hm4
Adora2atm1Jfc/Adora2atm1Jfc involves: 129S4/SvJae * C57BL/6 MGI:3622794
cn5
Adktm2Bois/Adktm2Bois
Adora2atm1Jfc/Adora2atm1Jfc
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:5816717
cx6
Adora2atm1Jfc/Adora2atm1Jfc
Drd2tm1Low/Drd2tm1Low
involves: 129 * C57BL/6 MGI:3625472


Genotype
MGI:5473699
hm1
Allelic
Composition
Adora2atm1Jfc/Adora2atm1Jfc
Genetic
Background
B6.129S4-Adora2atm1Jfc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adora2atm1Jfc mutation (2 available); any Adora2a mutation (36 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• cell proliferation is increased in all major cell types across entire pulmonary arterial walls, including smooth muscle, endothelium cells and fibroblasts compared to wild-type mice
• pulmonary arteries exhibit swelling and hypertrophy of endothelial and smooth muscle cells, with abundance of cytoplasm and an increase in intracytoplasmic vesicles
• pulmonary artery endothelium contains more Weibel-Palade bodies than in wild-type, indicating activation of endothelial cells
• cytoplasm of pulmonary artery smooth muscle cells contains numerous filaments and dense bodies, indicating activation of smooth muscle cells
• mutants exhibit enhanced hyperplasia of pulmonary artery fibroblasts, as indicated by an increase in fibroblasts seen outside the external elastic laminae and more clustered collagaen fibers deposition in adventitia pulmonary arterial walls
• mutants exhibit hypertrophy of pulmonary resistance vessels with increased wall thickness and area
• mice exhibit evidence of pulmonary vascular remodeling, showing fibroblast, smooth muscle and endothelium cell hypertrophy
• however, mutants do not exhibit pulmonary edema, lung inflammation, fibrosis or thickening of the alveolar septa
• pulmonary artery wall exhibits increased smooth muscle cell hypertorphy
• the mean Fulton index (ratio of right ventricle over left ventricle plus septum) is higher in mutants than wild-type mice at 14-16 weeks of age, indicating hypertrophic right ventricles
• mice exhibit a 44.8% increase in right ventricular systolic pressure at 14-16 weeks of age
• however, mean systolic blood pressure and heart rate are normal
• following chronic exposure to hypoxia, mutants show an exacerbated elevation in right ventricular systolic pressure
• mice develop pulmonary arterial hypertension without affecting systemic circulation or heart rate
• following chronic exposure to hypoxia, mutants show exacerbated elevation in right ventricular systolic pressure, hypertrophy of pulmonary resistance vessels, and increased cell proliferation in pulmonary resistance vessels compared to wild-type mice, indicating a further increase in pulmonary hypertension under hypoxic conditions
• however, mutants do not show any features of hypertensive nephropathy

muscle
• pulmonary artery wall exhibits increased smooth muscle cell hypertorphy
• the mean Fulton index (ratio of right ventricle over left ventricle plus septum) is higher in mutants than wild-type mice at 14-16 weeks of age, indicating hypertrophic right ventricles

respiratory system
• mutants exhibit hypertrophy of pulmonary resistance vessels with increased wall thickness and area
• mice exhibit evidence of pulmonary vascular remodeling, showing fibroblast, smooth muscle and endothelium cell hypertrophy
• however, mutants do not exhibit pulmonary edema, lung inflammation, fibrosis or thickening of the alveolar septa

growth/size/body
• the mean Fulton index (ratio of right ventricle over left ventricle plus septum) is higher in mutants than wild-type mice at 14-16 weeks of age, indicating hypertrophic right ventricles




Genotype
MGI:3625471
hm2
Allelic
Composition
Adora2atm1Jfc/Adora2atm1Jfc
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adora2atm1Jfc mutation (2 available); any Adora2a mutation (36 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• mutants do not show lower levels of locomotor stimulation in response to a Grm5 antagonist, MPEP, whereas compared to wild-type controls




Genotype
MGI:3622795
hm3
Allelic
Composition
Adora2atm1Jfc/Adora2atm1Jfc
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adora2atm1Jfc mutation (2 available); any Adora2a mutation (36 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• homozygotes do not display enhanced locomotor activation (over activation seen after the first exposure) after repeated administration of amphetamines (J:106215)
• however, locomotor responses to dopamine receptor D1A and dopamine receptor 2 agonists is similar to wild-type mice (J:106215)
• single exposure amphetamine stimulated increases in locomotor activity are reduced compared to wild-type mice (J:107988)

nervous system
• 24 hours after middle cerebral arterial occlusion neurological deficit scores for homozygotes are reduced by 50-60% compared to wild-type mice
• after middle cerebral arterial occlusion total infarct volume is reduced by 30% compared to wild-type mice
• after middle cerebral arterial occlusion infarct volume in the cerebral cortex and striatum are reduced by 33% and 27%, respectively

cardiovascular system
N
• basal mean arterial blood pressure, absolute blood flow, and cortical cerebral blood flow before, during. and after middle cerebral arterial occlusion is similar to wild-type mice

homeostasis/metabolism
• homozygotes do not display increased expression of dynorphin mRNA in the striatum after repeated administration of amphetamines
• 24 hours after middle cerebral arterial occlusion neurological deficit scores for homozygotes are reduced by 50-60% compared to wild-type mice
• after middle cerebral arterial occlusion total infarct volume is reduced by 30% compared to wild-type mice
• after middle cerebral arterial occlusion infarct volume in the cerebral cortex and striatum are reduced by 33% and 27%, respectively




Genotype
MGI:3622794
hm4
Allelic
Composition
Adora2atm1Jfc/Adora2atm1Jfc
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adora2atm1Jfc mutation (2 available); any Adora2a mutation (36 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• no significant increase in wakefulness is seen in homozygotes after injection of 15 mg/kg, 10 mg/kg, or 5 mg/kg caffeine, unlike wild-type mice (J:99612)
• however, baseline circadian sleep-wake profiles are identical to wild-type (J:99612)
• single exposure amphetamine or cocaine stimulated increases in locomotor activity are reduced compared to wild-type mice (J:107988)
• however, amphetamine stimulated increases in fine movement are not significantly different from wild-type (J:107988)
• reduced spontaneous activity most prominently in the dark cycle; however normal locomotor circadian rhythms are seen (J:107988)

homeostasis/metabolism
• 24 hours after middle cerebral arterial occlusion neurological deficit scores for homozygotes are reduced by 50-60% compared to wild-type mice
• after middle cerebral arterial occlusion total infarct volume is reduced by 26% using hematoxylin and eosin staining or by 77% using TTC staining (marker of intact cellular metabolism) compared to wild-type mice

nervous system
N
• morphology of cortex and striatum appears normal (J:73594)
• dopaminergic innervation is normal (J:107988)
• 24 hours after middle cerebral arterial occlusion neurological deficit scores for homozygotes are reduced by 50-60% compared to wild-type mice
• after middle cerebral arterial occlusion total infarct volume is reduced by 26% using hematoxylin and eosin staining or by 77% using TTC staining (marker of intact cellular metabolism) compared to wild-type mice

cardiovascular system
N
• basal mean arterial blood pressure, absolute blood flow, and cortical cerebral blood flow before, during. and after middle cerebral arterial occlusion is similar to wild-type mice

vision/eye
N
• normal growth in the anterior segment and normal pupil size
• sclera contains denser collagen fibrils with reduced diameter
• mice develop greater myopia than wild-type mice, that is associated with increases in vitreous chamber depth and axial length from P28 to P56




Genotype
MGI:5816717
cn5
Allelic
Composition
Adktm2Bois/Adktm2Bois
Adora2atm1Jfc/Adora2atm1Jfc
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adktm2Bois mutation (0 available); any Adk mutation (50 available)
Adora2atm1Jfc mutation (2 available); any Adora2a mutation (36 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• mice exhibit a resistance to stress-induced (placement in novel environment) seizures

behavior/neurological
N
• mice exhibit normal associative learning and contextual learning
• mice exhibit a resistance to stress-induced (placement in novel environment) seizures




Genotype
MGI:3625472
cx6
Allelic
Composition
Adora2atm1Jfc/Adora2atm1Jfc
Drd2tm1Low/Drd2tm1Low
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adora2atm1Jfc mutation (2 available); any Adora2a mutation (36 available)
Drd2tm1Low mutation (1 available); any Drd2 mutation (70 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• mutants do not show lower levels of locomotor stimulation in response to a Grm5 antagonist, MPEP, whereas compared to wild-type controls





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last database update
04/16/2024
MGI 6.23
The Jackson Laboratory