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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Camk2a-cre)1Szi
transgene insertion 1, Scott Zeitlin
MGI:2177768
Summary 8 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Ercc6tm1Gvh/Ercc6tm1Gvh
Xpatm1Gvh/Xpatm1Hvs
Tg(Camk2a-cre)1Szi/0
involves: 129P2/OlaHsd * C57BL/6J * CBA MGI:5312300
cn2
Htttm1Szi/Htttm2Szi
Tg(Camk2a-cre)1Szi/0
involves: 129S/SvEv * 129S1/Sv * C57BL/6 * CBA MGI:3605769
cn3
Bdnftm1Sieg/Bdnftm1Sieg
Tg(Camk2a-cre)1Szi/0
involves: 129S/SvEv * C57BL/6 * CBA MGI:2678292
cn4
Rap1atm1Morz/Rap1atm1Morz
Rap1btm1Morz/Rap1btm1Morz
Tg(Camk2a-cre)1Szi/?
involves: 129S/SvEv * C57BL/6J * CBA MGI:3777607
cn5
Adora2atm1Dyj/Adora2atm1Dyj
Tg(Camk2a-cre)1Szi/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:3625435
cn6
Adora2atm1Dyj/Adora2atm1.1Dyj
Tg(Camk2a-cre)1Szi/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:3625463
cn7
Hif1atm3Rsjo/Hif1atm3Rsjo
Tg(Camk2a-cre)1Szi/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:4418498
cn8
Oxtrtm1.1Wsy/Oxtrtm1.1Wsy
Tg(Camk2a-cre)1Szi/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA * SJL MGI:3801098


Genotype
MGI:5312300
cn1
Allelic
Composition
Ercc6tm1Gvh/Ercc6tm1Gvh
Xpatm1Gvh/Xpatm1Hvs
Tg(Camk2a-cre)1Szi/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ercc6tm1Gvh mutation (1 available); any Ercc6 mutation (78 available)
Tg(Camk2a-cre)1Szi mutation (0 available)
Xpatm1Gvh mutation (0 available); any Xpa mutation (22 available)
Xpatm1Hvs mutation (4 available); any Xpa mutation (22 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Dilated ventricles and brain atrophy in Ercc6tm1Gvh/Ercc6tm1Gvh Xpatm1Gvh/Xpatm1Hvs Tg(Camk2a-cre)1Szi/0 mice

mortality/aging
• between 12 and 22 months

nervous system
• from 9 to 12 months of age, mice exhibit seizure behavior characterized by episodes of immobility unlike control mice
• at 6 to 12 months of age, mice exhibit atrophy in the telencephalon (cortex, hippocampus, caudate-putamen and septum) unlike control mice
• atrophic at 6 to 12 months of age
• atrophic at 6 to 12 months of age
• mild atrophy at 6 months of age
• severe atrophy in older mice
• atrophic at 65 weeks
• at 6 to 12 months of age

behavior/neurological
• at 12 months of age
• from 9 to 12 months of age, mice exhibit seizure behavior characterized by episodes of immobility unlike control mice

growth/size/body
• at 9 to 12 months of age
• at 9 to 12 months of age

immune system

hematopoietic system




Genotype
MGI:3605769
cn2
Allelic
Composition
Htttm1Szi/Htttm2Szi
Tg(Camk2a-cre)1Szi/0
Genetic
Background
involves: 129S/SvEv * 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Htttm1Szi mutation (0 available); any Htt mutation (179 available)
Htttm2Szi mutation (0 available); any Htt mutation (179 available)
Tg(Camk2a-cre)1Szi mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• die between 11 and 13 months of age

growth/size/body
• smaller than controls at weaning and at P60

behavior/neurological
• abnormal limb clasping at P60 that becomes progressively more severe such that mice curl their body upon clasping and maintain the posture for several seconds following return to cage
• exhibit a slight tremor at 10-12 months of age
• exhibit motor defects in mutants subjected to cage-top rotation test and elevated wire rod hanging test
• noticeably hypoactive at 10-12 months of age

nervous system
• gliosis is seen throughout the forebrain in older mutants
• reactive astocytosis in the entorhinal cortex, striatum, and frontal cortex at 4 and 10 months of age
• 4 and 8 month old mutants exhibit neurodegeneration in the external capsule fibre tracts and in fibre bundles of the internal capsule within the striatum, in the amygdala and in both the frontal and dorsal cortex

reproductive system
• exhibit a reduction in the number of spermatocytes and round spermatids in the seminiferous tubules and in mature motile sperm in the lumen of the epididymis
• disorganized and contain fewer spermatocytes and round spermatids compared to controls
• testis is about 50% the weight of controls

endocrine/exocrine glands
• disorganized and contain fewer spermatocytes and round spermatids compared to controls
• testis is about 50% the weight of controls

cellular
• exhibit a reduction in the number of spermatocytes and round spermatids in the seminiferous tubules and in mature motile sperm in the lumen of the epididymis

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Huntington's disease DOID:12858 OMIM:143100
J:65520




Genotype
MGI:2678292
cn3
Allelic
Composition
Bdnftm1Sieg/Bdnftm1Sieg
Tg(Camk2a-cre)1Szi/0
Genetic
Background
involves: 129S/SvEv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bdnftm1Sieg mutation (0 available); any Bdnf mutation (41 available)
Tg(Camk2a-cre)1Szi mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• significant decrease in the magnitude of LTP induced by 200 Hz tetanic stimulation, such that the mean field EPSP measured 1 hour after induction of LTP is enhanced to only 145% of its pretetanus level in mutants compared to 198% enhancement in controls
• the enhancement of FM 1-43 (a fluorescent marker of synaptic vesicle cycling) release from presynaptic terminals seen in controls during high-frequency (200 Hz) tetanic stimulation is blocked in mutants; rate of FM 1-43 release during low-frequency (50 Hz) tetanic stimulation is normal
• mutants exhibit a smaller magnitude of LTP 1 hour following theta burst stimulation, with an enhancement in the fEPSP to 136.7% of it's initial value compared to 166% in controls




Genotype
MGI:3777607
cn4
Allelic
Composition
Rap1atm1Morz/Rap1atm1Morz
Rap1btm1Morz/Rap1btm1Morz
Tg(Camk2a-cre)1Szi/?
Genetic
Background
involves: 129S/SvEv * C57BL/6J * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rap1atm1Morz mutation (2 available); any Rap1a mutation (23 available)
Rap1btm1Morz mutation (2 available); any Rap1b mutation (32 available)
Tg(Camk2a-cre)1Szi mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• protein levels of Rap1 are reduced by 89.4% in the cortex and 38.7% in the thalamus
• synaptic efficacy in cortical but not thalamic input to the lateral amygdale is 2.5-fold higher than in wild-type mice
• current-voltage relationships for AMPAR and NMDAR currents are similar to wild-type mice
• in the cortico-amygdala pathway, spike-timing-dependent LTP was substantially reduced with only 2 of 7 cells showing a LTP response compared to 8 of 11 cells from wild-type
• EPSC evoked by minimal stimulation of cortical inputs into the lateral amygdale reveals increased release of glutamate
• mice do not demonstrate PPF in cortical inputs to the lateral amygdale before or after long-term potentiation

behavior/neurological
• mice have reduced fear learning as measured by freezing to a conditioned stimulus both 3 hours and 48 hours after training with a moderately adversive unconditioned stimulus
• there is no difference in fear learning compared to wild-type mice when a more severe unconditioned stimulus is used in training




Genotype
MGI:3625435
cn5
Allelic
Composition
Adora2atm1Dyj/Adora2atm1Dyj
Tg(Camk2a-cre)1Szi/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adora2atm1Dyj mutation (1 available); any Adora2a mutation (36 available)
Tg(Camk2a-cre)1Szi mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• in response to the adenosine (A2a) agonist KW-6002, locomotion is induced in male control animals but not in conditional knockout mice
• enhancement of fine movement behavior in controls is observed in response to amphetamine treatment but not in knockouts




Genotype
MGI:3625463
cn6
Allelic
Composition
Adora2atm1Dyj/Adora2atm1.1Dyj
Tg(Camk2a-cre)1Szi/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adora2atm1.1Dyj mutation (0 available); any Adora2a mutation (36 available)
Adora2atm1Dyj mutation (1 available); any Adora2a mutation (36 available)
Tg(Camk2a-cre)1Szi mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• daily treatment with amphetamine enhances locomotor responses in male control mice but does not affect male mutants; 1 week after cessation of treatment robust locomotor sensitization persists in controls
• control mice exhibit greater locomotor response when treated with a Grm5 antagonist, MPEP, than forebrain-specific knockout mice (J:102700)
• in response to the adenosine (A2a) agonist KW-6002, locomotion is induced in male control animals but not in conditional knockout mice (J:104338)
• enhancement of fine movement behavior in male controls is observed in response to amphetamine treatment but not in knockouts (J:104338)




Genotype
MGI:4418498
cn7
Allelic
Composition
Hif1atm3Rsjo/Hif1atm3Rsjo
Tg(Camk2a-cre)1Szi/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1atm3Rsjo mutation (3 available); any Hif1a mutation (48 available)
Tg(Camk2a-cre)1Szi mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• following transient middle cerebral artery occlusion

nervous system
• mice exhibit a slight reduction in cerebral cortex microvascular density compared with Hif1atm3Rsjo homozygotes
• following bilateral common carotid artery occlusion, mice exhibit decreased neuronal damage compared to in similarly treated Hif1atm3Rsjo homozygotes
• following transient middle cerebral artery occlusion, mice exhibit increased infarct size, increased neurological deficit scores, and mortality compared with similarly treated Hif1atm3Rsjo homozygotes
• 4 days after transient middle cerebral artery occlusion, infarct size is larger than in similarly treated Hif1atm3Rsjo homozygotes
• the neuroprotective effects on infarct size and neurological deficit scores of 3,4-dihydroxybenzoic acid, deferoxamine (DFO), and DP following transient middle cerebral artery occlusion is decreased compared to in similarly treated Hif1atm3Rsjo homozygotes
• however, mice still respond to neuroprotective hypoxia with reduced infarct volume at shorter exposure periods than wild-type mice
• uncommon

homeostasis/metabolism
• the neuroprotective effects on infarct size and neurological deficit scores of 3,4-dihydroxybenzoic acid, deferoxamine (DFO), and DP following transient middle cerebral artery occlusion is decreased compared to in similarly treated Hif1atm3Rsjo homozygotes
• following bilateral common carotid artery occlusion, mice exhibit decreased neuronal damage compared to in similarly treated Hif1atm3Rsjo homozygotes
• following transient middle cerebral artery occlusion, mice exhibit increased infarct size, increased neurological deficit scores, and mortality compared with similarly treated Hif1atm3Rsjo homozygotes
• 4 days after transient middle cerebral artery occlusion, infarct size is larger than in similarly treated Hif1atm3Rsjo homozygotes
• the neuroprotective effects on infarct size and neurological deficit scores of 3,4-dihydroxybenzoic acid, deferoxamine (DFO), and DP following transient middle cerebral artery occlusion is decreased compared to in similarly treated Hif1atm3Rsjo homozygotes
• however, mice still respond to neuroprotective hypoxia with reduced infarct volume at shorter exposure periods than wild-type mice

behavior/neurological
• following transient middle cerebral artery occlusion, mice exhibit increased neurological deficit scores compared with similarly treated Hif1atm3Rsjo homozygotes
• the neuroprotective effects on infarct size and neurological deficit scores of 3,4-dihydroxybenzoic acid, deferoxamine (DFO), and DP following transient middle cerebral artery occlusion is decreased compared to in similarly treated Hif1atm3Rsjo homozygotes

cardiovascular system
• mice exhibit a slight reduction in cerebral cortex microvascular density compared with Hif1atm3Rsjo homozygotes




Genotype
MGI:3801098
cn8
Allelic
Composition
Oxtrtm1.1Wsy/Oxtrtm1.1Wsy
Tg(Camk2a-cre)1Szi/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Oxtrtm1.1Wsy mutation (1 available); any Oxtr mutation (40 available)
Tg(Camk2a-cre)1Szi mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• weigh less than control mice
• weight discrepancy relative to controls increases with age

endocrine/exocrine glands
N
• normal milk production

behavior/neurological
• less time spend by males investigating either familiar or novel females during second trials
• 5-trial recognition studies indicated no difference between mutant mice and controls





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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory