Phenotypes associated with this allele

• Allele Symbol: Calr^tm1Star
• Allele Name: targeted mutation 1, Rene St-Arnaud
• Allele ID: MGI:2183263
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Calr^tm1Star/Calr^tm1Star	either: (involves: 129S1/Sv * 129X1/SvJ) or (involves: 129S1/Sv * 129X1/SvJ * C57BL)	MGI:3044167

Genotype
MGI:3044167

hm1

• Allelic Composition: Calr^tm1Star/Calr^tm1Star
• Genetic Background: either: (involves: 129S1/Sv * 129X1/SvJ) or (involves: 129S1/Sv * 129X1/SvJ * C57BL)

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

mortality/aging

lethality throughout fetal growth and development, complete penetrance ( J:61550 )

• one-third of homozygous null mice died at E14.5

• the remaining two-thirds died between E14.5 and birth

cardiovascular system

trabecula carnea hypoplasia ( J:61550 )

• at E14.5, 50% of homozygotes displayed reduced ventricular trabeculation

abnormal interventricular septum muscular part morphology ( J:61550 )

• at E14.5, 50% of homozygotes had a thinner muscular septum

thin ventricular wall ( J:61550 )

• at E14.5, 50% of homozygotes had thin ventricular walls

ventricular cardiomyopathy ( J:61550 )

• at E14.5, 50% of homozygotes displayed cardiomyopathy

cellular

abnormal cell physiology ( J:61550 )

• mutant MEFs displayed normal survival under various endoplasmic reticulum stress conditions

• in tunicamycin-treated cells, viability after 48 hours was even slightly improved in mutant MEFs

abnormal cell adhesion ( J:73539 )

• mutant MEFs displayed impaired integrin-mediated adhesion to fibronectin and vitronectin

increased cardiomyocyte apoptosis ( J:61550 )

• cardiomyopathy was associated with increased apoptosis of cardiomyocytes

• in vitro, embryoid bodies derived from homozygous null ES cells were unable to differentiate into contracting cardiomyocytes

abnormal cell migration ( J:61550 )

• MEFs and neuronal cells derived from homozygous null embryos exhibited migratory defects

• migration behavior was dependent on the concentration of extracellular matrix substrate

embryo

incomplete rostral neuropore closure ( J:61550 )

• 16% of homozygous embryos displayed a failure in cranial neural tube closure which resulted in hypercellularity

• no closure defects were detected at the level of the spine

muscle

trabecula carnea hypoplasia ( J:61550 )

• at E14.5, 50% of homozygotes displayed reduced ventricular trabeculation

ventricular cardiomyopathy ( J:61550 )

• at E14.5, 50% of homozygotes displayed cardiomyopathy

increased cardiomyocyte apoptosis ( J:61550 )

• cardiomyopathy was associated with increased apoptosis of cardiomyocytes

• in vitro, embryoid bodies derived from homozygous null ES cells were unable to differentiate into contracting cardiomyocytes

nervous system

incomplete rostral neuropore closure ( J:61550 )

• 16% of homozygous embryos displayed a failure in cranial neural tube closure which resulted in hypercellularity

• no closure defects were detected at the level of the spine

exencephaly ( J:61550 )

• 16% of homozygous embryos displayed exencephaly

growth/size/body

omphalocele ( J:61550 )

• 50% of homozygous null embryos surviving until E16.5 failed to close the ventral body wall, resulting in omphalocele

failure of ventral body wall closure ( J:61550 )

• 50% of homozygous null embryos surviving until E16.5 failed to close the ventral body wall, resulting in omphalocele