About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(CMV-Gja1)BClo
transgene insertion B, Cecilia W Lo
MGI:3620921
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cx1
Gja1tm1Kdr/Gja1tm1Kdr
Tg(CMV-Gja1)BClo/0
involves: 129S1/Sv * 129X1/SvJ * SJL/J * SWR/J MGI:3622647
tg2
Tg(CMV-Gja1)BClo/Tg(CMV-Gja1)BClo involves: SJL/J * SWR/J MGI:3622646
tg3
Tg(CMV-Gja1)BClo/0 involves: CD-1 * SJL/J * SWR/J MGI:3622645
tg4
Tg(CMV-Gja1)BClo/0 involves: SJL/J * SWR/J MGI:3622644


Genotype
MGI:3622647
cx1
Allelic
Composition
Gja1tm1Kdr/Gja1tm1Kdr
Tg(CMV-Gja1)BClo/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * SJL/J * SWR/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gja1tm1Kdr mutation (1 available); any Gja1 mutation (59 available)
Tg(CMV-Gja1)BClo mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 3 of 10 die at P12

cardiovascular system
• exhibit a network of fiber-like projections over the surface of the heart that are not seen in controls
• conotruncal enlargement of the right ventricle with multiple bulges
• blood flow into the right ventricular tract shows varying degrees of obstruction, with the most severe obstruction leading to backflow of the injected dye into the atrial chambers

muscle
• conotruncal enlargement of the right ventricle with multiple bulges

growth/size/body
• conotruncal enlargement of the right ventricle with multiple bulges




Genotype
MGI:3622646
tg2
Allelic
Composition
Tg(CMV-Gja1)BClo/Tg(CMV-Gja1)BClo
Genetic
Background
involves: SJL/J * SWR/J
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 40% die suddenly by 6 months of age showing no visible signs of illness
• premature lethality is particularly common among pregnant and nursing females
• proportion of transgenics arising from hemizygous matings is decreased to 54% at weaning

growth/size/body
• small size reflects a growth deficiency, not a developmental delay, as embryos are at the same somite stage of development as controls

cardiovascular system
• unusual dilation of vessels
• apical myocardium of the right ventricle exhibits a spongy appearance in fetal/neonatal hearts
• trabeculae are disorganized in the right ventricle of fetal/neonatal hearts
• show abnormalities in the disposition of surface coronary vasculature
• abnormalities in the deployment of the subepicardial coronary vasculature are frequently seen
• heart dysmorphology associated with overall shape
• near absence of the compact layer in the right ventricle of fetal/neonatal hearts
• hypertrophy of the interventricular septum in fetal/neonatal hearts
• enlargement of the conotruncal region of the right ventricle, seen as an outpouching which extends along the right atrioventricular groove
• narrowing of the pulmonary outflow region caused by apparent hypertrophy of the right ventricle
• some hearts exhibit aneurysm-like pouchings of the ventricular lumen

nervous system
• in severely affected embryos, the neural plate encompassing the midbrain/anterior hindbrain fails to elevate and exhibits a flat configuration with a convex curvature and abnormal curling along the dorsolateral margin
• 24% incidence of neural tube defects at E8.5-E14.5
• exhibit neural tube closure defects, however by late gestation, nearly all embryos appear normal, suggesting that neural tube closure eventually proceeds to completion
• embryos at E8 with a mild neural tube defects exhibit small openings along the roof of the presumptive midbrain/hindbrain
• severely affected E8-8.5 embryos exhibit complete failure of neural tube closure between closure sites 2 and 4
• collapsed appearance of brain ventricles at E10.5-11.5
• partial or complete exencephaly is seen in a few embryos late in gestation
• both mutants with and without neural tube defects exhibit peripheral ganglia and nerve perturbations
• trigeminal ganglion is reduced with little or no evidence for the formation of the ophthalmic, maxillary, and mandibular nerves
• nerve projections from the facial-acoustico (VII/VIII) ganglia are reduced
• roots of the hypoglossal nerve are poorly developed
• spinal nerves are poorly developed

muscle
• apical myocardium of the right ventricle exhibits a spongy appearance in fetal/neonatal hearts
• trabeculae are disorganized in the right ventricle of fetal/neonatal hearts
• near absence of the compact layer in the right ventricle of fetal/neonatal hearts

embryo
• in severely affected embryos, the neural plate encompassing the midbrain/anterior hindbrain fails to elevate and exhibits a flat configuration with a convex curvature and abnormal curling along the dorsolateral margin
• 24% incidence of neural tube defects at E8.5-E14.5
• exhibit neural tube closure defects, however by late gestation, nearly all embryos appear normal, suggesting that neural tube closure eventually proceeds to completion
• embryos at E8 with a mild neural tube defects exhibit small openings along the roof of the presumptive midbrain/hindbrain
• severely affected E8-8.5 embryos exhibit complete failure of neural tube closure between closure sites 2 and 4




Genotype
MGI:3622645
tg3
Allelic
Composition
Tg(CMV-Gja1)BClo/0
Genetic
Background
involves: CD-1 * SJL/J * SWR/J
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• viability is reduced, with fewer hemizygous mice detected at weaning

nervous system
• 9% incidence of neural tube defects at E8.5-E14.5

cellular
• increase in gap junction communication in embryos

embryo
• 9% incidence of neural tube defects at E8.5-E14.5




Genotype
MGI:3622644
tg4
Allelic
Composition
Tg(CMV-Gja1)BClo/0
Genetic
Background
involves: SJL/J * SWR/J
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants showing no visible signs of illness sometimes die suddenly
• lethality is more common among pregnant and nursing females

nervous system
• 14% incidence of neural tube defects at E8.5-E14.5
• incomplete penetrance
• both mutants with and without neural tube defects exhibit peripheral ganglia and nerve perturbations that are seen in homozygotes, although less severely

cardiovascular system
• exhibit similar, although less severe, cardiac abnormalities as seen in homozygotes

embryo
• 14% incidence of neural tube defects at E8.5-E14.5
• incomplete penetrance





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
04/30/2024
MGI 6.23
The Jackson Laboratory