All Phenotypes Tcf21<tm2Eno> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Tcf21^tm2Eno/Tcf21^tm2Eno	involves: 129 * Black Swiss	MGI:2174758
hm2	Tcf21^tm2Eno/Tcf21^tm2Eno	involves: 129 * C57BL/6	MGI:5444119
cx3	Msc^tm1Eno/Msc^tm1Eno Tcf21^tm2Eno/Tcf21^tm2Eno	involves: 129 * Black Swiss	MGI:3655699
cx4	Msc^tm1Eno/Msc⁺ Tcf21^tm2Eno/Tcf21^tm2Eno	involves: 129 * Black Swiss	MGI:3655867
cx5	Msc^tm1Eno/Msc^tm1Eno Tcf21^tm2Eno/Tcf21⁺	involves: 129 * Black Swiss	MGI:3655869

Allelic Composition	Tcf21^tm2Eno/Tcf21^tm2Eno
Genetic Background	involves: 129 * Black Swiss

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tcf21^tm2Eno mutation (0 available); any Tcf21 mutation (14 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

neonatal lethality, complete penetrance ( J:64068 )

• homozygotes are born alive but die within 5-10 min after birth

homeostasis/metabolism

cyanosis ( J:64068 )

• homozygotes become cyanotic shortly after birth

respiratory system

abnormal branching involved in lung morphogenesis ( J:64068 )

• mutant lung epithelia fail to undergo branching morphogenesis

pulmonary hypoplasia ( J:64068 )

• mutant lungs are severely hypoplastic

absent pulmonary alveoli ( J:64068 )

• homozygotes show absence of respiratory alveoli

respiratory distress ( J:64068 )

• newborn homozygotes have difficulty in breathing and display gasping motions

hematopoietic system

abnormal spleen development ( J:64068 )

• splenic precursors are specified, as shown by normal expression of early markers of spleen development in the splenic anlage at E12.5; however, the mutant splenic anlage fails to expand and, in its absence, the splenic primordium undergoes apoptotic cell death

absent spleen ( J:64068 )

• newborn homozygotes display complete absence of a spleen

• in contrast, the stomach and pancreas are properly located

renal/urinary system

renal glomerulus atrophy ( J:64068 )

• homozygotes display atrophic kidney glomeruli

abnormal kidney development ( J:64068 )

renal hypoplasia ( J:64068 )

• mutant kidneys are severely hypoplastic

impaired branching involved in ureteric bud morphogenesis ( J:64068 )

• mutant kidney epithelia fail to undergo branching morphogenesis

immune system

abnormal spleen development ( J:64068 )

absent spleen ( J:64068 )

• newborn homozygotes display complete absence of a spleen

• in contrast, the stomach and pancreas are properly located

integument

pallor ( J:64068 )

• homozygotes become pale shortly after birth

Allelic Composition	Tcf21^tm2Eno/Tcf21^tm2Eno
Genetic Background	involves: 129 * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tcf21^tm2Eno mutation (0 available); any Tcf21 mutation (14 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cardiovascular system

abnormal heart morphology ( J:185552 )

• regions of epicardial detachment are noted around midgestation

• at E13.5 and later, mutants have fewer Tcf21-positive interstitial cells with no significant changes in apoptosis or cell proliferation, suggesting defective migration of epicardial cells into the myocardium (epicardial EMT defects)

• epicardial-derived cells form coronary vascular smooth muscle cells but do not form cardiac fibroblasts; this leads to extracellular matrix (ECM) deficiencies in mutant hearts (lower concentrations of some ECM proteins)

thin myocardium ( J:185552 )

• reduced myocardial thickness

abnormal heart apex morphology ( J:185552 )

• absence of a distinct heart apex

increased heart right atrium size ( J:185552 )

abnormal heart shape ( J:185552 )

• embryonic heart is dysmorphic and lacks distinct apex

hemopericardium ( J:185552 )

• embryos have blood in pericardial cavity, observed at E17.5 and later

homeostasis/metabolism

hemopericardium ( J:185552 )

• embryos have blood in pericardial cavity, observed at E17.5 and later

muscle

thin myocardium ( J:185552 )

• reduced myocardial thickness

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

neonatal lethality, complete penetrance ( J:111337 )

• double homozygotes are born alive, but similar to single Tcf21^tm2Eno homozygotes, they die within minutes after birth

muscle

abnormal masticatory muscle morphology ( J:111337 )

• most double homozygotes show a complete absence of the major muscles of mastication, not observed in either single homozygote

absent masseter muscle ( J:111337 )

• most double homozygotes show a complete absence of the masseter muscle

abnormal pterygoid muscle morphology ( J:111337 )

• atrophic pterygoid myofibers are found to persist unilaterally in a subset of double homozygotes

absent pterygoid muscle ( J:111337 )

• most double homozygotes show a complete absence of the medial and lateral pterygoid muscles

absent temporalis muscle ( J:111337 )

• most double homozygotes show a complete absence of the temporalis muscle

abnormal myogenesis ( J:111337 )

• at E10.5, TUNEL labeling indicates that first branchial arch muscle precursor cells undergo apoptosis resulting in ablation of masticatory muscles

• notably, other first arch-derived muscles, e.g. the anterior digastric and mylohyoid, which do not function in mastication, are present and trunk muscles appear unaffected

diaphragmatic hernia ( J:111337 )

• double homozygotes exhibit diaphragmatic hernia with visceral organs being displaced into the chest

craniofacial

abnormal masticatory muscle morphology ( J:111337 )

• most double homozygotes show a complete absence of the major muscles of mastication, not observed in either single homozygote

absent masseter muscle ( J:111337 )

• most double homozygotes show a complete absence of the masseter muscle

abnormal pterygoid muscle morphology ( J:111337 )

• atrophic pterygoid myofibers are found to persist unilaterally in a subset of double homozygotes

absent pterygoid muscle ( J:111337 )

• most double homozygotes show a complete absence of the medial and lateral pterygoid muscles

absent temporalis muscle ( J:111337 )

• most double homozygotes show a complete absence of the temporalis muscle

cleft secondary palate ( J:111337 )

• double homozygotes exhibit cleft palate

abnormal palatal shelf elevation ( J:111337 )

• palatal shelves do not elevate or elevate unilaterally (Fig. 3c)

digestive/alimentary system

cleft secondary palate ( J:111337 )

• double homozygotes exhibit cleft palate

abnormal palatal shelf elevation ( J:111337 )

• palatal shelves do not elevate or elevate unilaterally (Fig. 3c)

growth/size/body

abnormal masticatory muscle morphology ( J:111337 )

• most double homozygotes show a complete absence of the major muscles of mastication, not observed in either single homozygote

absent masseter muscle ( J:111337 )

• most double homozygotes show a complete absence of the masseter muscle

abnormal pterygoid muscle morphology ( J:111337 )

• atrophic pterygoid myofibers are found to persist unilaterally in a subset of double homozygotes

absent pterygoid muscle ( J:111337 )

• most double homozygotes show a complete absence of the medial and lateral pterygoid muscles

absent temporalis muscle ( J:111337 )

• most double homozygotes show a complete absence of the temporalis muscle

cleft secondary palate ( J:111337 )

• double homozygotes exhibit cleft palate

abnormal palatal shelf elevation ( J:111337 )

• palatal shelves do not elevate or elevate unilaterally (Fig. 3c)

Allelic Composition	Msc^tm1Eno/Msc⁺ Tcf21^tm2Eno/Tcf21^tm2Eno
Genetic Background	involves: 129 * Black Swiss

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Msc^tm1Eno mutation (1 available); any Msc mutation (11 available)
Tcf21^tm2Eno mutation (0 available); any Tcf21 mutation (14 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

muscle

muscle phenotype ( J:111337 )

N	• unlike double homozygotes, mice heterozygous for Msc^tm1Eno and homozygous for Tcf21^tm2Eno exhibit no morphological defects in first branchial arch-derived masticatory skeletal muscles

Allelic Composition	Msc^tm1Eno/Msc^tm1Eno Tcf21^tm2Eno/Tcf21⁺
Genetic Background	involves: 129 * Black Swiss

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

normal phenotype

no abnormal phenotype detected ( J:111337 )

• unlike double homozygotes, mice homozygous for Msc^tm1Eno and heterozygous for Tcf21^tm2Eno are viable and exhibit no morphological defects in first branchial arch-derived masticatory skeletal muscles

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)
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