Phenotypes associated with this allele

• Allele Symbol: Postn^tm1Jmol
• Allele Name: targeted mutation 1, Jeffery D Molkentin
• Allele ID: MGI:3819350
• Summary: 3 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Postn^tm1Jmol/Postn^tm1Jmol	involves: 129S/SvEv	MGI:4837386
hm2	Postn^tm1Jmol/Postn^tm1Jmol	involves: 129/Sv * C57BL/6	MGI:3819378
cx3	Myh6^tm1Jse/Myh6^+ Postn^tm1Jmol/Postn^tm1Jmol	involves: 129S/SvEv * 129X1/SvJ	MGI:4837387

Genotype
MGI:4837386

hm1

• Allelic Composition: Postn^tm1Jmol/Postn^tm1Jmol
• Genetic Background: involves: 129S/SvEv

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

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:165269 )

N • cyclosporine A-treated mice exhibit normal hypertrophic cardiomyopathy

Genotype
MGI:3819378

hm2

• Allelic Composition: Postn^tm1Jmol/Postn^tm1Jmol
• Genetic Background: involves: 129/Sv * C57BL/6

cardiovascular system

small heart ( J:140301 )

• slightly

abnormal response to cardiac infarction ( J:140301 )

• following induced myocardial infarct, mice exhibit less of an increase in the number of fibroblasts in the left ventricle compared to in wild-type mice

• following induced myocardial infarct, mice exhibit an increase in death during the first 10 days and a 2-fold increase in the rate of ventricular wall rupture but reduced fibrosis and overall size of scaring compared to similarly treated wild-type mice

• however, mice maintain better cardiac function compared to wild-type mice over the 8 weeks following the initial scar formation

homeostasis/metabolism

abnormal response to cardiac infarction ( J:140301 )

• following induced myocardial infarct, mice exhibit less of an increase in the number of fibroblasts in the left ventricle compared to in wild-type mice

• following induced myocardial infarct, mice exhibit an increase in death during the first 10 days and a 2-fold increase in the rate of ventricular wall rupture but reduced fibrosis and overall size of scaring compared to similarly treated wild-type mice

• however, mice maintain better cardiac function compared to wild-type mice over the 8 weeks following the initial scar formation

decreased susceptibility to injury ( J:140301 )

• following transverse aortic constriction to induce pressure overload, mice exhibit less cardiac hypertrophy with reduced myocyte cross-section diameter and increased ventricular function after 8 weeks compared to similarly treated wild-type mice

• however, initial response during the first 2 weeks after pressure overload is normal

cellular

abnormal cell adhesion ( J:140301 )

• isolated fibroblasts exhibit reduced adhesion to neonatal cardiomyocytes compared to wild-type fibroblasts

growth/size/body

decreased body weight ( J:140301 )

• as adults

Genotype
MGI:4837387

cx3

• Allelic Composition: Myh6^tm1Jse/Myh6⁺; Postn^tm1Jmol/Postn^tm1Jmol
• Genetic Background: involves: 129S/SvEv * 129X1/SvJ

cardiovascular system

cardiac fibrosis ( J:165269 )

• cyclosporine A-treated mice exhibit reduced myocardial fibrosis than in similarly treated Myh6^tm1Jse homozygotes

abnormal cardiovascular system physiology ( J:165269 )

• cyclosporine A-treated mice exhibit a 2.4-fold reduction in non-myocyte cell proliferation compared with similarly treated Myh6^tm1Jse homozygotes but remains higher than in similarly treated wild-type mice

homeostasis/metabolism

decreased physiological sensitivity to xenobiotic ( J:165269 )

• cyclosporine A-treated mice exhibit a modest, but not significantly, reduction in maximal left ventricular wall thickness compared with similarly treated Myh6^tm1Jse homozygotes

• cyclosporine A-treated mice exhibit reduced myocardial fibrosis than in similarly treated Myh6^tm1Jse homozygotes

• cyclosporine A-treated mice exhibit a 2.4-fold reduction in non-myocyte cell proliferation compared with similarly treated Myh6^tm1Jse homozygotes but remains higher than in similarly treated wild-type mice