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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Cdh2tm1Hyn
targeted mutation 1, Richard Hynes
MGI:1861181
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Cdh2tm1Hyn/Cdh2tm1Hyn involves: 129S2/SvPas MGI:2170969
cn2
Cdh2tm1Glr/Cdh2tm1Hyn
A1cfTg(Myh6-cre/Esr1*)1Jmk/A1cf+
involves: 129S6/SvEvTac * C57BL/6J * FVB/N MGI:3580162
cx3
Cdh11tm1Mta/Cdh11tm1Mta
Cdh2tm1Hyn/Cdh2tm1Hyn
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 MGI:2662271


Genotype
MGI:2170969
hm1
Allelic
Composition
Cdh2tm1Hyn/Cdh2tm1Hyn
Genetic
Background
involves: 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdh2tm1Hyn mutation (1 available); any Cdh2 mutation (50 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

embryo
• blood vessels in the yolk sac are not appropriately formed
• rarely turn completely from the lordotic to the fetal position
• significantly delayed by E9.5 and are equivalent in size to normal E9 embryos
• undulation of the neural tube
• at E8.5, somites are small, irregularly shaped, and less cohesive (J:37888)
• at E9.0, epithelial somites are smaller and irregular in size and shape (J:58409)
• epithelial somites are cleaved into rostral and caudal halves immediately after somite formation (J:58409)
• however, most of these fragmented somites maintain epithelial, vesicle-like structures (J:58409)
• exhibit separation of the mesodermal and endodermal cell layers of the yolk sac; however, points of contact are still maintained between the two cell layers

cardiovascular system
• blood vessels in the yolk sac are not appropriately formed
• cardiac myoocytes surround the endocardium and are unable to develop a normal myocardium
• cardiac myocytes tend to disaggregate
• all embryos examined between E9 and E10 exhibit a malformed heart tube
• myocytes dissociated from heart tubes form loose aggregates that contract weakly in vitro compared to strong beating aggregates in wild-type
• seen as early as E8.5
• expanded pericardial cavity occupies much of the amniotic cavity

growth/size/body
• seen as early as E8.5
• significantly delayed by E9.5 and are equivalent in size to normal E9 embryos

nervous system
• undulation of the neural tube

muscle
• cardiac myoocytes surround the endocardium and are unable to develop a normal myocardium
• cardiac myocytes tend to disaggregate




Genotype
MGI:3580162
cn2
Allelic
Composition
Cdh2tm1Glr/Cdh2tm1Hyn
A1cfTg(Myh6-cre/Esr1*)1Jmk/A1cf+
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (5 available); any A1cf mutation (39 available)
Cdh2tm1Glr mutation (1 available); any Cdh2 mutation (50 available)
Cdh2tm1Hyn mutation (1 available); any Cdh2 mutation (50 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants die about 2 months after tamoxifen treatment

cardiovascular system
• after tamoxifen treatment enlarged hyperchromatic myocyte nuclei are seen
• after tamoxifen treatment intercalated disc structures and intercellular space are absent
• after tamoxifen treatment sarcomeres appear distorted and compressed with wider, less dense Z-lines
• after tamoxifen treatment intercalated disc structures are absent
• modest dilation of the atria after tamoxifen treatment
• after tamoxifen treatment hearts appear elongated and flacid
• modest dilation of the ventricles after tamoxifen treatment
• modest dilation of the ventricles after tamoxifen treatment
• eft ventricular end-diastolic and end-systolic volume in the cavity are increased and left ventricular ejection fraction is decreased
• about 5 weeks after tamoxifen treatment, mutant heart rate is significantly reduced
• about 6 weeks after tamoxifen treatment, 2 mutants showed abrupt onset of ventricular tachyarrhythmia followed by sudden death
• about 6 weeks after tamoxifen treatment, 2 mutants showed abrupt onset of ventricular tachyarrhythmia followed by sudden death
• tachyarrhythmia is initiated by premature ventricular depolarization

muscle
• after tamoxifen treatment enlarged hyperchromatic myocyte nuclei are seen
• after tamoxifen treatment intercalated disc structures and intercellular space are absent
• after tamoxifen treatment sarcomeres appear distorted and compressed with wider, less dense Z-lines
• after tamoxifen treatment intercalated disc structures are absent
• eft ventricular end-diastolic and end-systolic volume in the cavity are increased and left ventricular ejection fraction is decreased




Genotype
MGI:2662271
cx3
Allelic
Composition
Cdh11tm1Mta/Cdh11tm1Mta
Cdh2tm1Hyn/Cdh2tm1Hyn
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdh11tm1Mta mutation (1 available); any Cdh11 mutation (42 available)
Cdh2tm1Hyn mutation (1 available); any Cdh2 mutation (50 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryo
• at E9.0, double mutant embryos display a more severe disorganization and fragmentation of the epithelial somites than single Cdh2tm1Hyn embryos
• each epithelial somite is cleaved into rostral and caudal halves just after somite formation, as in single Cdh2tm1Hyn embryos; however, in double mutant embryos, each half is further fragmented into smaller clusters, and the caudal and rostral compartments tend to separate from each other





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last database update
03/19/2024
MGI 6.23
The Jackson Laboratory