About   Help   FAQ
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




Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support. 		last database update
10/29/2024
MGI 6.24 		The Jackson Laboratory