Phenotypes associated with this allele

• Allele Symbol: Atp2a2^tm1.1Iemr
• Allele Name: targeted mutation 1.1, Ole Sejersted
• Allele ID: MGI:4415164
• Summary: 3 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Atp2a2^tm1.1Iemr/Atp2a2^+ Myl2^tm1(cre)Krc/Myl2^+	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6Crl * C57BL/6J	MGI:4415177
cn2	Atp2a2^tm1.1Iemr/Atp2a2^tm1.1Iemr Tg(Myhca-cre)1Lrsn/0	involves: 129P2/OlaHsd * C57BL/6Crl * FVB	MGI:4415178
cn3	Atp2a2^tm1.1Iemr/Atp2a2^tm1.1Iemr A1cf^Tg(Myh6-cre/Esr1*)1Jmk/A1cf^+	involves: 129P2/OlaHsd * C57BL/6J * FVB/N	MGI:4441305

Genotype
MGI:4415177

cn1

• Allelic Composition: Atp2a2^tm1.1Iemr/Atp2a2⁺; Myl2^tm1(cre)Krc/Myl2⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6Crl * C57BL/6J

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

cardiovascular system

cardiovascular system phenotype ( J:155628 )

N • mice exhibit normal heart weight and cardiac function

Genotype
MGI:4415178

cn2

• Allelic Composition: Atp2a2^tm1.1Iemr/Atp2a2^tm1.1Iemr; Tg(Myhca-cre)1Lrsn/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6Crl * FVB

mortality/aging

embryonic lethality during organogenesis, complete penetrance ( J:155628 )

• although alive at E10.5, embryos die by E11.5

Genotype
MGI:4441305

cn3

• Allelic Composition: Atp2a2^tm1.1Iemr/Atp2a2^tm1.1Iemr; A1cf^{Tg(Myh6-cre/Esr1*)1Jmk}/A1cf⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J * FVB/N

cardiovascular system

cardiovascular system phenotype ( J:157143 )

N • tamoxifen-treated mice do not exhibit myocardial disarray or necrosis

abnormal heart left atrium morphology ( J:157143 )

• 4 and 7 weeks after tamoxifen treatment, left atrial diameter is increased compared to in Atp2a2^tm1.1Iemr homozygotes

dilated heart atrium ( J:157143 )

• after tamoxifen treatment

enlarged heart ( J:157143 )

• after tamoxifen treatment

abnormal cardiovascular system physiology ( J:157143 )

• tamoxifen-treated mice exhibit an increase in the time constant of isovolumetric pressure decay compared with Atp2a2^tm1.1Iemr homozygotes

• 7 weeks after tamoxifen treatment, mice exhibit diastolic dysfunction compared with Atp2a2^tm1.1Iemr homozygotes

decreased cardiac output ( J:157143 )

• 4 and 7 weeks after tamoxifen treatment

decreased cardiac muscle contractility ( J:157143 )

• 4 weeks after tamoxifen treatment, mice exhibit reduced contractile function compared with Atp2a2^tm1.1Iemr homozygotes as determined by Doppler imaging

• at low stimulation frequency, cardiomyocytes from tamoxifen-treated mice exhibit reduced contraction magnitude compared with similarly treated cardiomyocytes from Atp2a2^tm1.1Iemr homozygotes

• 7 weeks after tamoxifen treatment, fractional shortening is reduced compared to in Atp2a2^tm1.1Iemr homozygotes

• 4 and 7 weeks after tamoxifen treatment, end-diastolic pressure compared to in Atp2a2^tm1.1Iemr homozygotes

abnormal heart left ventricle pressure ( J:157143 )

• 4 and 7 weeks after tamoxifen treatment, mice exhibit reduced maximum positive and minimum derivatives of the left ventricular pressure compared with Atp2a2^tm1.1Iemr homozygotes

decreased heart rate ( J:157143 )

• 4 and 7 weeks after tamoxifen treatment, anesthetized mice exhibit decreased heart rate compared with Atp2a2^tm1.1Iemr homozygotes

abnormal myocardial fiber physiology ( J:157143 )

• cardiomyocytes from tamoxifen-treated mice exhibit reduced magnitude of calcium ion transients and prolonged time to half decay of calcium ion transients compared with similarly treated cardiomyocytes from Atp2a2^tm1.1Iemr homozygotes

• when stimulated at a 6 Hz frequency, cardiomyocytes from tamoxifen-treated mice exhibit shorter diastolic sarcomere length and a greater increase in the contractile response per unit during systole compared with similarly treated cardiomyocytes from Atp2a2^tm1.1Iemr homozygotes

• during the slow decline of caffeine transients in the presence of nickel ions, cardiomyocytes from tamoxifen-treated mice exhibit shorter sarcomere length compared with similarly treated cardiomyocytes from Atp2a2^tm1.1Iemr homozygotes

• 4 weeks after tamoxifen treatment, cardiomyocytes exhibit reduced sarcoplasmic reticulum calcium ion content compared with cardiomyocytes from Atp2a2^tm1.1Iemr homozygotes

• 7 weeks after treatment with tamoxifen, mice exhibit reduced maximal rate of cardiomyocyte relaxation compared with Atp2a2^tm1.1Iemr homozygotes

decreased systemic arterial systolic blood pressure ( J:157143 )

• 7 weeks after tamoxifen treatment

homeostasis/metabolism

increased circulating noradrenaline level ( J:157143 )

• in tamoxifen-treated mice at 4 and 7 weeks

muscle

decreased cardiac muscle contractility ( J:157143 )

• 4 weeks after tamoxifen treatment, mice exhibit reduced contractile function compared with Atp2a2^tm1.1Iemr homozygotes as determined by Doppler imaging

• at low stimulation frequency, cardiomyocytes from tamoxifen-treated mice exhibit reduced contraction magnitude compared with similarly treated cardiomyocytes from Atp2a2^tm1.1Iemr homozygotes

• 7 weeks after tamoxifen treatment, fractional shortening is reduced compared to in Atp2a2^tm1.1Iemr homozygotes

• 4 and 7 weeks after tamoxifen treatment, end-diastolic pressure compared to in Atp2a2^tm1.1Iemr homozygotes

growth/size/body

enlarged heart ( J:157143 )

• after tamoxifen treatment