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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID 		Plntm1Egk
targeted mutation 1, Evangelia G Kranias
MGI:2158357
Summary 14 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
 		Plntm1Egk/Plntm1Egk involves: 129S2/SvPas MGI:3653917
hm2
 		Plntm1Egk/Plntm1Egk involves: 129S2/SvPas * CF-1 MGI:3041404
hm3
 		Plntm1Egk/Plntm1Egk involves: 129S2/SvPas * CF-1 * FVB/N MGI:3799198
cx4
 		Atp2a2tm1Fwuy/Atp2a2tm1Fwuy
Plntm1Egk/Plntm1Egk 		involves: 129 * FVB/N * Swiss MGI:3662928
cx5
 		Hprt1tm1Dhm/Hprt1tm1Dhm
Plntm1Egk/Plntm1Egk 		involves: 129P2/OlaHsd * 129S2/SvPas MGI:3653918
cx6
 		Hprt1tm1Dhm/Y
Plntm1Egk/Plntm1Egk 		involves: 129P2/OlaHsd * 129S2/SvPas MGI:3653919
cx7
 		Plntm1Egk/Plntm1Egk
Zdhhc16tm1Goff/Zdhhc16tm1Goff 		involves: 129S1/Sv * 129S2/SvPas MGI:5907022
cx8
 		Plntm1Egk/Plntm1Egk
Tg(Myh6-Pln)11Egk/? 		involves: 129S2/SvPas MGI:5051959
cx9
 		Plntm1Egk/Plntm1Egk
Tg(Myh6-Pln)22Egk/? 		involves: 129S2/SvPas MGI:5051956
cx10
 		Plntm1Egk/Plntm1Egk
Tg(Myh6-Pln)1Egk/? 		involves: 129S2/SvPas MGI:5051960
cx11
 		Plntm1Egk/Plntm1Egk
Tnnt2tm2.1Feah/Tnnt2+ 		involves: 129S2/SvPas * 129S6/SvEvTac * FVB/N MGI:5910773
cx12
 		Plntm1Egk/Plntm1Egk
Tg(Myh6*)140Lnwd/0 		involves: 129S2/SvPas * CBA * CF-1 * FVB/N MGI:3799199
cx13
 		Csrp3tm1Crni/Csrp3tm1Crni
Plntm1Egk/Plntm1Egk 		involves: 129S2/SvPas * CF-1 MGI:3037269
cx14
 		Plntm1Egk/Plntm1Egk
Tg(Myh6/tetO-Tnnc1*I61Q)1Jmol/0
Tg(Myh6-tTA)55Rbns/0 		involves: 129S2/SvPas * FVB MGI:5897396


Genotype
MGI:3653917
hm1
Allelic
Composition		 Plntm1Egk/Plntm1Egk
Genetic
Background		 involves: 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plntm1Egk mutation (7 available); any Pln mutation (16 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
increased cardiac muscle contractility ( J:106044 )
• isolated cardiac myocytes exhibit a significant increase in fractional cell shortening and higher dL/dT values
abnormal cardiac muscle relaxation ( J:106044 )
• isolated cardiac myocytes exhibit higher relaxation rates (-dL/dt) than wild-type
atrial fibrillation ( J:212640 )
• induced by atrial burst pacing that is not prevented by 1,4-benzothiazepine (Rycal S107)-treatment
abnormal myocardial fiber physiology ( J:106044 )
• under baseline conditions, left ventricular myocytes exhibit an enhanced calcium transient amplitude and faster calcium transient decays
• left ventricular myocytes do not show an increase in the intracellular calcium transient amplitudes or accelerated calcium transient decays when treated with isoproterenol as is seen in wild-type

muscle
increased cardiac muscle contractility ( J:106044 )
• isolated cardiac myocytes exhibit a significant increase in fractional cell shortening and higher dL/dT values
abnormal cardiac muscle relaxation ( J:106044 )
• isolated cardiac myocytes exhibit higher relaxation rates (-dL/dt) than wild-type




Genotype
MGI:3041404
hm2
Allelic
Composition		 Plntm1Egk/Plntm1Egk
Genetic
Background		 involves: 129S2/SvPas * CF-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plntm1Egk mutation (7 available); any Pln mutation (16 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
increased cardiac muscle contractility ( J:39745 , J:59967 )
• no increased contractility in response to beta-adrenergic agonists (J:39745)
• large force developed at low frequencies of stimulation but more like controls at higher frequencies (J:59967)
• no acceleration of time to peak tension with increasing frequency of stimulation, similar observation for relaxation time (J:59967)
• declining rate of force development with increased frequency of stimulation (J:59967)
abnormal heart left ventricle pressure ( J:39745 )
• diastolic and end diastolic pressures were decreased
• rates of pressure development were increased
• systolic intraventricular pressure increased

muscle
increased cardiac muscle contractility ( J:39745 , J:59967 )
• no increased contractility in response to beta-adrenergic agonists (J:39745)
• large force developed at low frequencies of stimulation but more like controls at higher frequencies (J:59967)
• no acceleration of time to peak tension with increasing frequency of stimulation, similar observation for relaxation time (J:59967)
• declining rate of force development with increased frequency of stimulation (J:59967)




Genotype
MGI:3799198
hm3
Allelic
Composition		 Plntm1Egk/Plntm1Egk
Genetic
Background		 involves: 129S2/SvPas * CF-1 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plntm1Egk mutation (7 available); any Pln mutation (16 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
increased heart weight ( J:134706 )
• the heart weight to body weight ratio is 10% greater compared to controls

growth/size/body
increased heart weight ( J:134706 )
• the heart weight to body weight ratio is 10% greater compared to controls




Genotype
MGI:3662928
cx4
Allelic
Composition		 Atp2a2tm1Fwuy/Atp2a2tm1Fwuy
Plntm1Egk/Plntm1Egk
Genetic
Background		 involves: 129 * FVB/N * Swiss
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atp2a2tm1Fwuy mutation (0 available); any Atp2a2 mutation (76 available)
Plntm1Egk mutation (7 available); any Pln mutation (16 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
growth/size/body
increased heart weight ( J:110974 )
• in double homozygous mice, heart weight/body weight ratios and heart weight/tibial length ratios are increased compared to wild-type
cardiac hypertrophy ( J:110974 )
• in double homozygous mice at 12-16 weeks, concentric hypertrophy was aggravated compared to single Atp2a2tm1Fwuy homozygous mice

mortality/aging
premature death ( J:110974 )
• the life span of mutant mice was severely shortened at 496 average age in days

cardiovascular system
increased myocardial fiber size ( J:110974 )
• the cardiomyocyte dimensions in double homozygous mice were increased to a much larger extent than in single Atp2a2tm1Fwuy homozygous mice
globular heart ( J:110974 )
• the hearts from double homozygous mice were more hypertrophic and balloon-shaped than the heart from single Atp2a2tm1Fwuy homozygous mice
increased heart weight ( J:110974 )
• in double homozygous mice, heart weight/body weight ratios and heart weight/tibial length ratios are increased compared to wild-type
cardiac hypertrophy ( J:110974 )
• in double homozygous mice at 12-16 weeks, concentric hypertrophy was aggravated compared to single Atp2a2tm1Fwuy homozygous mice
thick ventricular wall ( J:110974 )
• in double homozygous mice at 12-16 weeks, echocardiographic measurements showed thicker posterior wall than single Atp2a2tm1Fwuy homozygous mice
increased heart left ventricle wall thickness ( J:110974 )
• cardiac sections showed a larger LV mass-measured as cross-sectional area
• LV wall thickening was not the result of increased interstitial fibrosis
abnormal cardiac output ( J:110974 )
• beta-adrenergic stimulation in double homozygous mice failed to increase the cardiac output
decreased cardiac stroke volume ( J:110974 )
• maximal and minimal LV volume and stroke volume appeared lower in double homozygous mice at 12-16 weeks
abnormal cardiac muscle relaxation ( J:110974 )
• impaired LV relaxation assessed by dP/dt min in double homozygous mice at 12-16 weeks compared to wild-type mice
• contractility assessed by dP/dt max were normal
decreased heart rate ( J:110974 )
• in double homozygous mice at 12-16 weeks compared to wild-type
congestive heart failure ( J:110974 )
• two out of 16 double homozygous mice died after completing running performance test on a rodent treadmill displaying clinical signs of congestive heart failure
• beta-adrenergic stimulation impaired LV contractility and relaxation and caused acute heart failure during the procedure

behavior/neurological
abnormal locomotor activation ( J:110974 )
• the spontaneous activity was severely reduced in double homozygous mice at 12-16 weeks of age compared to wild-type and single Atp2a2tm1Fwuy homozygous mice

homeostasis/metabolism
abnormal calcium ion homeostasis ( J:110974 )
• the maximal pumping capacity of sarcoplasmic reticulum calcium ion uptake was reduced by 50% in cardiac homogenate of homozygous mutant mice

muscle
increased myocardial fiber size ( J:110974 )
• the cardiomyocyte dimensions in double homozygous mice were increased to a much larger extent than in single Atp2a2tm1Fwuy homozygous mice
abnormal cardiac muscle relaxation ( J:110974 )
• impaired LV relaxation assessed by dP/dt min in double homozygous mice at 12-16 weeks compared to wild-type mice
• contractility assessed by dP/dt max were normal




Genotype
MGI:3653918
cx5
Allelic
Composition		 Hprt1tm1Dhm/Hprt1tm1Dhm
Plntm1Egk/Plntm1Egk
Genetic
Background		 involves: 129P2/OlaHsd * 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hprt1tm1Dhm mutation (0 available); any Hprt1 mutation (1279 available)
Plntm1Egk mutation (7 available); any Pln mutation (16 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
increased cardiac muscle contractility ( J:106044 )
• isolated cardiac myocytes exhibit enhanced fractional cell shortening and higher dL/dT values compared to wild-type, however this shortening and dL/dT values are less than that seen in the single homozygous Pln mutant mouse
abnormal cardiac muscle relaxation ( J:106044 )
• isolated cardiac myocytes exhibit higher relaxation rates (-dL/dt) than wild-type but lower than that seen in single homozygous Pln mutant mice
abnormal myocardial fiber physiology ( J:106044 )
• under baseline conditions, left ventricular myocytes exhibit faster calcium transient decays than wild-type, however they are slower than in single homozygous Pln mutant mice

muscle
increased cardiac muscle contractility ( J:106044 )
• isolated cardiac myocytes exhibit enhanced fractional cell shortening and higher dL/dT values compared to wild-type, however this shortening and dL/dT values are less than that seen in the single homozygous Pln mutant mouse
abnormal cardiac muscle relaxation ( J:106044 )
• isolated cardiac myocytes exhibit higher relaxation rates (-dL/dt) than wild-type but lower than that seen in single homozygous Pln mutant mice




Genotype
MGI:3653919
cx6
Allelic
Composition		 Hprt1tm1Dhm/Y
Plntm1Egk/Plntm1Egk
Genetic
Background		 involves: 129P2/OlaHsd * 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hprt1tm1Dhm mutation (0 available); any Hprt1 mutation (1279 available)
Plntm1Egk mutation (7 available); any Pln mutation (16 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
increased cardiac muscle contractility ( J:106044 )
• isolated cardiac myocytes exhibit enhanced fractional cell shortening and higher dL/dT values compared to wild-type, however this shortening and dL/dT values are less than that seen in the single homozygous Pln mutant mouse
abnormal cardiac muscle relaxation ( J:106044 )
• isolated cardiac myocytes exhibit higher relaxation rates (-dL/dt) than wild-type but lower than that seen in single homozygous Pln mutant mice
abnormal myocardial fiber physiology ( J:106044 )
• under baseline conditions, left ventricular myocytes exhibit faster calcium transient decays than wild-type, however they are slower than in single homozygous Pln mutant mice

muscle
increased cardiac muscle contractility ( J:106044 )
• isolated cardiac myocytes exhibit enhanced fractional cell shortening and higher dL/dT values compared to wild-type, however this shortening and dL/dT values are less than that seen in the single homozygous Pln mutant mouse
abnormal cardiac muscle relaxation ( J:106044 )
• isolated cardiac myocytes exhibit higher relaxation rates (-dL/dt) than wild-type but lower than that seen in single homozygous Pln mutant mice




Genotype
MGI:5907022
cx7
Allelic
Composition		 Plntm1Egk/Plntm1Egk
Zdhhc16tm1Goff/Zdhhc16tm1Goff
Genetic
Background		 involves: 129S1/Sv * 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plntm1Egk mutation (7 available); any Pln mutation (16 available)
Zdhhc16tm1Goff mutation (0 available); any Zdhhc16 mutation (25 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
mortality/aging
neonatal lethality, complete penetrance ( J:228307 )
• fail to survive to P2; however, almost all survive to birth

cardiovascular system
cardiovascular system phenotype ( J:228307 )
N
• double mutation rescues the histopathological defects (cardiomyocyte disarray, nuclear malformations, decreased sarcomere numbers) and bradycardia seen in Zdhhc16 null mice

vision/eye
abnormal eye development ( J:228307 )
• eye defects




Genotype
MGI:5051959
cx8
Allelic
Composition		 Plntm1Egk/Plntm1Egk
Tg(Myh6-Pln)11Egk/?
Genetic
Background		 involves: 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plntm1Egk mutation (7 available); any Pln mutation (16 available)
Tg(Myh6-Pln)11Egk mutation (1 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
abnormal cardiac muscle contractility ( J:66084 )
• ventricular myocytes exhibit increases in shortening fraction, rates of shortening and de-lengthening following maximal stimulation with the beta adrenergic agonist, isoproterenol, however, these increases are lower than increases experienced by controls
• basal cardiac function is similar to control
abnormal myocardial fiber physiology ( J:66084 )
• maximal isoproterenol stimulation has little effect on the Ca2+ amplitude peak and no effect on the decline of Ca2+ transient in myocytes

muscle
abnormal cardiac muscle contractility ( J:66084 )
• ventricular myocytes exhibit increases in shortening fraction, rates of shortening and de-lengthening following maximal stimulation with the beta adrenergic agonist, isoproterenol, however, these increases are lower than increases experienced by controls
• basal cardiac function is similar to control




Genotype
MGI:5051956
cx9
Allelic
Composition		 Plntm1Egk/Plntm1Egk
Tg(Myh6-Pln)22Egk/?
Genetic
Background		 involves: 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plntm1Egk mutation (7 available); any Pln mutation (16 available)
Tg(Myh6-Pln)22Egk mutation (1 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
cardiovascular system phenotype ( J:66084 )
N
• ventricular myocytes exhibit increases in shortening fraction, rates of shortening and de-lengthening following maximal stimulation with the beta adrenergic agonist, isoproterenol, however, these increases are similar to those observed in mice expressing Plntm1Egk Tg(Myh6-Pln)1Egk (wild type phospholambin)




Genotype
MGI:5051960
cx10
Allelic
Composition		 Plntm1Egk/Plntm1Egk
Tg(Myh6-Pln)1Egk/?
Genetic
Background		 involves: 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plntm1Egk mutation (7 available); any Pln mutation (16 available)
Tg(Myh6-Pln)1Egk mutation (1 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
cardiovascular system phenotype ( J:66084 )
N
• mutant mice appear phenotypically normal; transgene expression rescues cardiac function




Genotype
MGI:5910773
cx11
Allelic
Composition		 Plntm1Egk/Plntm1Egk
Tnnt2tm2.1Feah/Tnnt2+
Genetic
Background		 involves: 129S2/SvPas * 129S6/SvEvTac * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plntm1Egk mutation (7 available); any Pln mutation (16 available)
Tnnt2tm2.1Feah mutation (0 available); any Tnnt2 mutation (51 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
dilated heart left ventricle ( J:243725 )
• mice exhibit left ventricular dilatation
dilated cardiomyopathy ( J:243725 )
• dilated cardiomyopathy is similar to that seen in single Tnnt2 heterozygotes
decreased cardiac muscle contractility ( J:243725 )
• mice exhibit decreased fractional shortening

muscle
dilated cardiomyopathy ( J:243725 )
• dilated cardiomyopathy is similar to that seen in single Tnnt2 heterozygotes
decreased cardiac muscle contractility ( J:243725 )
• mice exhibit decreased fractional shortening




Genotype
MGI:3799199
cx12
Allelic
Composition		 Plntm1Egk/Plntm1Egk
Tg(Myh6*)140Lnwd/0
Genetic
Background		 involves: 129S2/SvPas * CBA * CF-1 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plntm1Egk mutation (7 available); any Pln mutation (16 available)
Tg(Myh6*)140Lnwd mutation (0 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
increased heart weight ( J:134706 )
• the heart weight to body weight ratio is 30% greater compared to controls

growth/size/body
increased heart weight ( J:134706 )
• the heart weight to body weight ratio is 30% greater compared to controls




Genotype
MGI:3037269
cx13
Allelic
Composition		 Csrp3tm1Crni/Csrp3tm1Crni
Plntm1Egk/Plntm1Egk
Genetic
Background		 involves: 129S2/SvPas * CF-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Csrp3tm1Crni mutation (0 available); any Csrp3 mutation (15 available)
Plntm1Egk mutation (7 available); any Pln mutation (16 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
cardiac hypertrophy ( J:58299 )
• indicated by a slight increase in the heart weight/body weight ratio
• heart structure is otherwise normalized compared to conditions in mice homozygous for with Csrp3Tm1Crni only
• more normal heart size
• normalized myofibrillar organization
• no fibrosis
• normal cardiac chamber dimensions as indicated by echocardiography
increased cardiac muscle contractility ( J:58299 )
• increased contractile properties similar to those of mice homozygous for Plntm1Egk only
• normalized left ventricular relaxation and diastolic function
decreased heart rate ( J:58299 )
• slightly decreased relative to wild-type

muscle
increased cardiac muscle contractility ( J:58299 )
• increased contractile properties similar to those of mice homozygous for Plntm1Egk only
• normalized left ventricular relaxation and diastolic function

growth/size/body
cardiac hypertrophy ( J:58299 )
• indicated by a slight increase in the heart weight/body weight ratio
• heart structure is otherwise normalized compared to conditions in mice homozygous for with Csrp3Tm1Crni only
• more normal heart size
• normalized myofibrillar organization
• no fibrosis
• normal cardiac chamber dimensions as indicated by echocardiography




Genotype
MGI:5897396
cx14
Allelic
Composition		 Plntm1Egk/Plntm1Egk
Tg(Myh6/tetO-Tnnc1*I61Q)1Jmol/0
Tg(Myh6-tTA)55Rbns/0
Genetic
Background		 involves: 129S2/SvPas * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plntm1Egk mutation (7 available); any Pln mutation (16 available)
Tg(Myh6/tetO-Tnnc1*I61Q)1Jmol mutation (1 available)
Tg(Myh6-tTA)55Rbns mutation (2 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
abnormal interventricular septum morphology ( J:234490 )
• improved compared with Tg(Myh6/tetO-Tnnc1*I61Q)1Jmol mice
increased heart weight ( J:234490 )
• more severe than in Tg(Myh6/tetO-Tnnc1*I61Q)1Jmol mice
increased heart left ventricle size ( J:234490 )
• as in Tg(Myh6/tetO-Tnnc1*I61Q)1Jmol mice
abnormal myocardial fiber physiology ( J:234490 )
• faster mechanical relaxation of myocyte contraction compared with Tg(Myh6/tetO-Tnnc1*I61Q)1Jmol
abnormal myocardial fiber calcium currents ( J:234490 )
• faster Ca2+ transient decay time compared with Tg(Myh6/tetO-Tnnc1*I61Q)1Jmol

growth/size/body
increased heart weight ( J:234490 )
• more severe than in Tg(Myh6/tetO-Tnnc1*I61Q)1Jmol mice




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Send questions and comments to User Support. 		last database update
11/12/2024
MGI 6.24 		The Jackson Laboratory