Phenotypes associated with this allele

• Allele Symbol: Rcan1^tm1Jmol
• Allele Name: targeted mutation 1, Jeffery D Molkentin
• Allele ID: MGI:3641540
• Summary: 4 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Rcan1^tm1Jmol/Rcan1^tm1Jmol	involves: 129 * C57BL/6	MGI:3652923
cx2	Rcan1^tm1Jmol/Rcan1^tm1Jmol Rcan2^tm1Jmol/Rcan2^tm1Jmol	involves: 129 * C57BL/6	MGI:3652924
cx3	Rcan1^tm1Jmol/Rcan1^tm1Jmol Tg(Myh6-Ppp3ca)37Eno/0	involves: 129 * C57BL/6 * FVB	MGI:3652925
cx4	Rcan1^tm1Jmol/Rcan1^tm1Jmol Rcan2^tm1Jmol/Rcan2^tm1Jmol Ppp3cb^tm1Jmk/Ppp3cb^tm1Jmk	involves: 129S6/SvEvTac * C57BL/6	MGI:3652928

Genotype
MGI:3652923

hm1

• Allelic Composition: Rcan1^tm1Jmol/Rcan1^tm1Jmol
• Genetic Background: involves: 129 * C57BL/6

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

growth/size/body

increased heart weight ( J:109586 )

• in response to pressure overload stimulus mutants show less increase in heart weight normalized to tibia length sompared to wild-type

decreased body weight ( J:109586 )

• homozygotes exhibit an ~10% decrease in body weight with age

cardiovascular system

abnormal myocardium layer morphology ( J:109586 )

• myocyte area (hypertrophy) is less than that observed in wild-type in response to pressure overload

increased heart weight ( J:109586 )

• in response to pressure overload stimulus mutants show less increase in heart weight normalized to tibia length sompared to wild-type

decreased response of heart to induced stress ( J:109586 )

• hypertrophy and increase in heart weight is reduced in response to pressure overload compared to wild-type

abnormal response to cardiac infarction ( J:109586 )

• myocardial damage is increased in mice after ischemia-reperfusion injury

reproductive system

reduced fertility ( J:109586 )

• mice exhibit reduced fertility with age

homeostasis/metabolism

decreased response of heart to induced stress ( J:109586 )

• hypertrophy and increase in heart weight is reduced in response to pressure overload compared to wild-type

abnormal response to cardiac infarction ( J:109586 )

• myocardial damage is increased in mice after ischemia-reperfusion injury

muscle

abnormal myocardium layer morphology ( J:109586 )

• myocyte area (hypertrophy) is less than that observed in wild-type in response to pressure overload

Genotype
MGI:3652924

cx2

• Allelic Composition: Rcan1^tm1Jmol/Rcan1^tm1Jmol; Rcan2^tm1Jmol/Rcan2^tm1Jmol
• Genetic Background: involves: 129 * C57BL/6

behavior/neurological

abnormal object recognition memory ( J:109586 )

• mice show subtle but significant impairment in working memory assessed by novel and familiar object recognition

hyperactivity ( J:109586 )

• mice show a significant increase in cumulative activity during light and dark conditions

immune system

decreased T cell proliferation ( J:109586 )

• in response to stimulation, total splenocytes show reduced proliferation

abnormal CD4-positive, alpha-beta T cell physiology ( J:109586 )

• after CD3 stimulation, increased apoptosis of CD4+ T cells is observed

abnormal cytokine secretion ( J:109586 )

• in response to stimulation, total splenocytes show reduced proliferation and Il2 production compared to wild-type

cardiovascular system

abnormal myocardium layer morphology ( J:109586 )

• mice do not display cardiac hypertrophy in response to 2 weeks of infusion of phenylephrine plus angiotensin II or 3 weeks of forced exercise unlike wild-type mice

decreased response of heart to induced stress ( J:109586 )

• cardiac function reveals partial protection from pressure overload stimulation decompensation induced by transverse aortic constriction compared to wild-type; cardiac hypertrophy is attenuated

abnormal response to cardiac infarction ( J:109586 )

• myocardial damage is increased in mice after ischemia-reperfusion injury

hematopoietic system

decreased T cell proliferation ( J:109586 )

• in response to stimulation, total splenocytes show reduced proliferation

abnormal CD4-positive, alpha-beta T cell physiology ( J:109586 )

• after CD3 stimulation, increased apoptosis of CD4+ T cells is observed

homeostasis/metabolism

decreased response of heart to induced stress ( J:109586 )

• cardiac function reveals partial protection from pressure overload stimulation decompensation induced by transverse aortic constriction compared to wild-type; cardiac hypertrophy is attenuated

abnormal response to cardiac infarction ( J:109586 )

• myocardial damage is increased in mice after ischemia-reperfusion injury

cellular

decreased T cell proliferation ( J:109586 )

• in response to stimulation, total splenocytes show reduced proliferation

muscle

abnormal myocardium layer morphology ( J:109586 )

• mice do not display cardiac hypertrophy in response to 2 weeks of infusion of phenylephrine plus angiotensin II or 3 weeks of forced exercise unlike wild-type mice

Genotype
MGI:3652925

cx3

• Allelic Composition: Rcan1^tm1Jmol/Rcan1^tm1Jmol; Tg(Myh6-Ppp3ca)37Eno/0
• Genetic Background: involves: 129 * C57BL/6 * FVB

cardiovascular system

increased heart weight ( J:109586 )

• Dscr1-deficiency induces a greater increase in cardiac hypertrophy in combination with Tg(Myh6-Ppp3ca)37Eno expression than in wild-type or Dscr1l1-deficiency with transgene expression

growth/size/body

increased heart weight ( J:109586 )

• Dscr1-deficiency induces a greater increase in cardiac hypertrophy in combination with Tg(Myh6-Ppp3ca)37Eno expression than in wild-type or Dscr1l1-deficiency with transgene expression

Genotype
MGI:3652928

cx4

• Allelic Composition: Rcan1^tm1Jmol/Rcan1^tm1Jmol; Rcan2^tm1Jmol/Rcan2^tm1Jmol; Ppp3cb^tm1Jmk/Ppp3cb^tm1Jmk
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6

behavior/neurological

hyperactivity ( J:109586 )

• mice show a significant increase in cumulative activity during light and dark conditions, even greater than that shown in Dscr1/Dscr1l1 knockouts

immune system

decreased T cell proliferation ( J:109586 )

• in response to stimulation, total splenocytes show reduced proliferation

abnormal CD4-positive, alpha beta T cell morphology ( J:109586 )

• T cell development is compromised in triple knockouts compared to wild-type, single or double knockouts; a reduction in number in the spleen is observed

abnormal CD8-positive, alpha beta T cell morphology ( J:109586 )

• T cell development is compromised in triple knockouts compared to wild-type, single or double knockouts; a reduction in number in the spleen is observed

abnormal CD4-positive, alpha-beta T cell physiology ( J:109586 )

• after CD3 stimulation, increased apoptosis of CD4+ T cells is observed

abnormal cytokine secretion ( J:109586 )

• in response to stimulation, total splenocytes show increased Il2 production compared to wild-type

hematopoietic system

decreased T cell proliferation ( J:109586 )

• in response to stimulation, total splenocytes show reduced proliferation

abnormal CD4-positive, alpha beta T cell morphology ( J:109586 )

• T cell development is compromised in triple knockouts compared to wild-type, single or double knockouts; a reduction in number in the spleen is observed

abnormal CD8-positive, alpha beta T cell morphology ( J:109586 )

• T cell development is compromised in triple knockouts compared to wild-type, single or double knockouts; a reduction in number in the spleen is observed

abnormal CD4-positive, alpha-beta T cell physiology ( J:109586 )

• after CD3 stimulation, increased apoptosis of CD4+ T cells is observed

cardiovascular system

decreased response of heart to induced stress ( J:109586 )

• cardiac function reveals partial protection from pressure overload stimulation decompensation induced by transverse aortic constriction compared to wild-type; cardiac hypertrophy is attenuated

homeostasis/metabolism

decreased response of heart to induced stress ( J:109586 )

• cardiac function reveals partial protection from pressure overload stimulation decompensation induced by transverse aortic constriction compared to wild-type; cardiac hypertrophy is attenuated

cellular

decreased T cell proliferation ( J:109586 )

• in response to stimulation, total splenocytes show reduced proliferation