Phenotypes associated with this allele

• Allele Symbol: Mapk14^tm1.2Otsu
• Allele Name: targeted mutation 1.2, Kinya Otsu
• Allele ID: MGI:3525576
• Summary: 4 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Mapk14^tm1.2Otsu/Mapk14^tm1.2Otsu	involves: C57BL/6J	MGI:3525857
cn2	Mapk14^tm1.1Otsu/Mapk14^tm1.2Otsu Slc6a3^tm1(cre)Xz/0	involves: 129S1/Sv * C57BL/6	MGI:5824896
cn3	Mapk14^tm1.2Otsu/Mapk14^tm1.2Otsu Tg(Myh6-cre)2182Mds/0	involves: C57BL/6J	MGI:3525858
cn4	Mapk14^tm1.2Otsu/Mapk14^tm1.2Otsu Tg(Col2a1-cre)1Bhr/0	involves: C57BL/6 * SJL	MGI:5532835

Genotype
MGI:3525857

hm1

• Allelic Composition: Mapk14^tm1.2Otsu/Mapk14^tm1.2Otsu
• Genetic Background: involves: C57BL/6J

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

normal phenotype

no abnormal phenotype detected ( J:95116 )

• appeared normal and indistinguishable from wild-type

Genotype
MGI:5824896

cn2

• Allelic Composition: Mapk14^tm1.1Otsu/Mapk14^tm1.2Otsu; Slc6a3^tm1(cre)Xz/0
• Genetic Background: involves: 129S1/Sv * C57BL/6

behavior/neurological

behavior/neurological phenotype ( J:226396 )

N • performance on the rotarod is similar to controls, although there is a slight trend toward improved performance

abnormal associative learning ( J:226396 )

• resistant to agonist U50,488-induced conditioned place aversion (CPA)

Genotype
MGI:3525858

cn3

• Allelic Composition: Mapk14^tm1.2Otsu/Mapk14^tm1.2Otsu; Tg(Myh6-cre)2182Mds/0
• Genetic Background: involves: C57BL/6J

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:95116 )

• 30% of mutants died one week after TAC induced pressure overload compared to 8% in controls

cardiovascular system

enlarged heart ( J:95116 )

• heart was larger than in controls after TAC induced pressure overload or adrenergic stimulation

increased heart weight ( J:95116 )

• heart weight, left ventricle weight, and average ratio of left ventricle weight to tibial length or body weight were significantly greater than in controls after TAC induced pressure overload, however no difference in cardiomyocyte cell area was observed

cardiac fibrosis ( J:95116 )

• observed intermuscular and perivascular fibrosis in mutants compared to only slight perivascular fibrosis in controls after TAC induced pressure overload

decreased cardiac muscle contractility ( J:95116 )

• mice exhibit normal cardiac function and structure under baseline conditions, however cardiac contractility was significantly reduced after thoracic transverse aortic constriction (TAC) induced pressure overload and chronic adrenergic stimulation

decreased heart left ventricle muscle contractility ( J:95116 )

• increased left ventricle end-diastolic and end-systolic diameters compared to controls after TAC induced pressure overload

increased response of heart to induced stress ( J:95116 )

• after TAC induced pressure overload, exhibit greater increases in mortality, heart size and weight, cardiac fibrosis, and cardiomyocyte apoptosis and decreased cardiac contractility compared to controls

muscle

decreased cardiac muscle contractility ( J:95116 )

• mice exhibit normal cardiac function and structure under baseline conditions, however cardiac contractility was significantly reduced after thoracic transverse aortic constriction (TAC) induced pressure overload and chronic adrenergic stimulation

decreased heart left ventricle muscle contractility ( J:95116 )

• increased left ventricle end-diastolic and end-systolic diameters compared to controls after TAC induced pressure overload

increased cardiomyocyte apoptosis ( J:95116 )

• the number of apoptotic cardiac myocytes was 3.7 times that in controls after TAC induced pressure overload and was also increased in response to chronic adrenergic stimulation

homeostasis/metabolism

increased response of heart to induced stress ( J:95116 )

• after TAC induced pressure overload, exhibit greater increases in mortality, heart size and weight, cardiac fibrosis, and cardiomyocyte apoptosis and decreased cardiac contractility compared to controls

cellular

increased cardiomyocyte apoptosis ( J:95116 )

• the number of apoptotic cardiac myocytes was 3.7 times that in controls after TAC induced pressure overload and was also increased in response to chronic adrenergic stimulation

growth/size/body

enlarged heart ( J:95116 )

• heart was larger than in controls after TAC induced pressure overload or adrenergic stimulation

increased heart weight ( J:95116 )

• heart weight, left ventricle weight, and average ratio of left ventricle weight to tibial length or body weight were significantly greater than in controls after TAC induced pressure overload, however no difference in cardiomyocyte cell area was observed

Genotype
MGI:5532835

cn4

• Allelic Composition: Mapk14^tm1.2Otsu/Mapk14^tm1.2Otsu; Tg(Col2a1-cre)1Bhr/0
• Genetic Background: involves: C57BL/6 * SJL

skeleton

short femur ( J:204227 )

♂ • at 6 months in male mice

short tibia ( J:204227 )

♂ • at 6 months in male mice

abnormal long bone epiphyseal plate proliferative zone ( J:204227 )

♂ • narrow in male mice

decreased width of hypertrophic chondrocyte zone ( J:204227 )

♂ • in male mice

decreased long bone epiphyseal plate size ( J:204227 )

♂ • in male mice

kyphosis ( J:204227 )

♂ • exaggerated in male mice at 6 months

small vertebrae ( J:204227 )

♂ • short at 6 months in male mice

growth/size/body

decreased body size ( J:204227 )

• by 3 to 4 weeks in female and male mice

decreased body length ( J:204227 )

• in male and female mice

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:204227 )

N • mice exhibit normal IGF1 serum levels

limbs/digits/tail

short femur ( J:204227 )

♂ • at 6 months in male mice

short tibia ( J:204227 )

♂ • at 6 months in male mice