Analysis Tools
cardiovascular system
| N |
• mice have normal heart conduction
|
|
Allele Symbol Allele Name Allele ID |
Gja1tm1Kwi targeted mutation 1, Klaus Willecke MGI:2445468 |
||||||||||||||||||||||||||||||||||||||||
| Summary |
9 genotypes
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice have normal heart conduction
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• ectopic ventricular beats and ventricle tachycardia are observed in 7 of 10 4-OHT treated mice
|
|
• 4-OHT treated mice have impaired conduction that is more pronounced on the right ventricle than the left ventricle
• longitudinal and transverse conduction is reduced on the right ventricle in 4-OHT treated mice
• transverse conduction is reduced on the left ventricle in 4-OHT treated mice
|
|
• following treatment with tamoxifen, ATP release from polymorphonuclear (PMN) cells is less than 15% of wild-type
|
|
• following treatment with tamoxifen, ATP release from polymorphonuclear (PMN) cells is less than 15% of wild-type
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• 4-OHT treated mice exhibit 40% reduction in coupling compared to un-induced and wild-type mice
|
|
• 4-OHT treated mice exhibit 40% reduction in coupling compared to un-induced and wild-type mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• cytoarchitecture of the adult brain appears normal; at 1.5 months, Bergmann glial processes show no morphologic abnormalites and Purkinje cell dendrite branching is normal
• cerebellar LTD induction and maintenance is not affected; no loss of astrocytes in the cerebellar cortex are detected in mutants
|
|
• intercellular coupling of Bergmann glial cells (through gap junctions) as indicated by dye injection is significantly reduced compared to Gja1tm1Kwi homozygous controls at 3.5 months
|
| N |
• no enhanced locomotor activity or increased exploratory behavior is observed in open field tests
• associative motor learning (in delay eyeblink conditioning) is similar between mutants and controls at 3-3.5 months
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• normal embryonic development and cardiac morphogenesis is observed
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice die between E16 and E18.5
|
|
• lymphatic vessel networks are less interconnected than in control mice
|
|
• fine vessels are absent
|
|
• severe
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• male mutants display normal testicular descent and genital tract development relative to control littermates
|
 |
• adult male mutants show loss and/or reduction of round or elongated spermatids
|
|
|
• adult male mutants show a significant reduction in the mean number of spermatogonia per seminiferous tubule relative to control littermates
|
|
|
• at P30, P60, P90, and P120, male mutants exhibit significantly reduced germ cell (spermatogonia) counts relative to control littermates
|
|
|
• no sperm are detected in the cauda epididymidis of mutant males
|
|
|
• most mutant Sertoli cells display immature or aberrant features, including rounded nuclei, and absence of tubular lumina and cytoplasmic vacuoles
• no mitotic figures are observed
|
|
|
• at P30, P60, P90, and P120, male mutants exhibit a significant increase in the mean number of Sertoli cells per seminiferous tubule relative to control littermates
|
|
|
• adult male mutants (P170) show smaller tubules with Sertoli cell (SC)-only syndrome and intratubular SC clusters
|
|
|
• a hyperplasia of interstitial Leydig cells is observed
|
|
|
• mutant testes are significantly smaller than those of control littermates
|
|
|
• adult male mutants (P60 to P120) show a drastic reduction in testis weight and relative testis weight (ratio between the weight of both testes to body weight) compared to control littermates
|
|
|
• 95% of mutant seminiferous tubules exhibit an arrest of spermatogenesis at the level of spermatogonia
• however, in 10 of 15 mutant males, ~5% of tubules exhibit qualitative normal spermatogenesis and few elongated spermatids
|
|
|
• no pups are produced when mutant males are mated with wild-type females, despite normal sexual behavior and presence of vaginal plugs
|
|
|
• most mutant Sertoli cells display immature or aberrant features, including rounded nuclei, and absence of tubular lumina and cytoplasmic vacuoles
• no mitotic figures are observed
|
|
|
• at P30, P60, P90, and P120, male mutants exhibit a significant increase in the mean number of Sertoli cells per seminiferous tubule relative to control littermates
|
|
|
• adult male mutants (P170) show smaller tubules with Sertoli cell (SC)-only syndrome and intratubular SC clusters
|
|
|
• a hyperplasia of interstitial Leydig cells is observed
|
|
|
• mutant testes are significantly smaller than those of control littermates
|
|
|
• adult male mutants (P60 to P120) show a drastic reduction in testis weight and relative testis weight (ratio between the weight of both testes to body weight) compared to control littermates
|
|
|
• adult male mutants show loss and/or reduction of round or elongated spermatids
|
|
|
• adult male mutants show a significant reduction in the mean number of spermatogonia per seminiferous tubule relative to control littermates
|
|
|
• at P30, P60, P90, and P120, male mutants exhibit significantly reduced germ cell (spermatogonia) counts relative to control littermates
|
|
|
• no sperm are detected in the cauda epididymidis of mutant males
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mutants lacking Gja1 in endothelium are viable, fertile, and show no abnormalities in the heart, brain, retina, pancreas, liver, kidney, spleen, testis, or blood pressure
|
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 04/23/2024 MGI 6.23 |
|
|
|
||