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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Myog-cre)1Eno
transgene insertion 1, Eric N Olson
MGI:3530558
Summary 18 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Hdac4tm1Eno/Hdac4tm2.1Eno
Hdac5tm1Eno/Hdac5tm1Eno
Tg(Myog-cre)1Eno/0
involves: 129 * 129S/SvEv * 129S2/SvPas MGI:4418137
cn2
Ppargc1atm2.1Brsp/Ppargc1atm2.1Brsp
Tg(Myog-cre)1Eno/0
involves: 129 * BALB/c * C57BL/6J * C57BL/6N MGI:5576914
cn3
Obscntm1Chen/Obscntm1Chen
Obsl1tm1.1Slan/Obsl1tm1.1Slan
Tg(Myog-cre)1Eno/0
involves: 129 * Black Swiss * C57BL/6 * SJL MGI:6476968
cn4
Obsl1tm1.1Slan/Obsl1tm1.1Slan
Tg(Myog-cre)1Eno/0
involves: 129 * Black Swiss * C57BL/6 * SJL MGI:6476965
cn5
Ppargc1atm2Brsp/Ppargc1a+
Tg(Myog-cre)1Eno/0
involves: 129 * C57BL/6 MGI:5576900
cn6
Cygbtm1Ppam/Cygbtm1Ppam
Tg(Myog-cre)1Eno/0
involves: 129 * C57BL/6 MGI:5575857
cn7
Ppargc1atm1Brsp/Ppargc1atm2Brsp
Tg(Myog-cre)1Eno/0
involves: 129 * C57BL/6 * FVB/N MGI:5576899
cn8
Srftm2.1Nor/Srftm2.1Nor
Tg(Myog-cre)1Eno/0
involves: 129P2/OlaHsd * C57BL/6 MGI:3530886
cn9
Mbnl1tm1Sws/Mbnl1tm1Sws
Mbnl2tm1Sws/Mbnl2tm1Sws
Tg(Myog-cre)1Eno/0
involves: 129S1/Sv * 129S1/SvImJ * C57BL MGI:5616749
cn10
Acacbtm1.1Lowl/Acacbtm1.1Lowl
Tg(Myog-cre)1Eno/0
involves: 129S4/SvJaeSor * 129S6/SvEvTac MGI:4450935
cn11
Mapk14tm1Lex/Mapk14tm1Lex
Tg(Myog-cre)1Eno/0
involves: 129S5/SvEvBrd MGI:4415790
cn12
Pnpla2tm1Eek/Pnpla2tm1Eek
Tg(Myog-cre)1Eno/0
involves: 129S * C57BL/6 MGI:5554580
cn13
Hdac4tm2.1Eno/Hdac4tm2.1Eno
Tg(Myog-cre)1Eno/0
involves: 129S/SvEv MGI:4418186
cn14
Mef2ctm1Eno/Mef2ctm2Eno
Tg(Myog-cre)1Eno/0
involves: 129S/SvEv * 129S7/SvEvBrd MGI:4418148
cn15
Mapk12tm1Lex/Mapk12tm1Lex
Tg(Myog-cre)1Eno/0
involves: 129S/SvEvBrd MGI:4415789
cn16
Mapk11tm2Lex/Mapk11tm2Lex
Tg(Myog-cre)1Eno/0
involves: 129S/SvEvBrd MGI:4415788
cn17
Gnai2tm2.1Lbi/Gnai2tm2.1Lbi
Gnai3tm1Lbi/Gnai3tm1Lbi
Tg(Myog-cre)1Eno/0
involves: 129S/SvEv * C57BL/6 MGI:5471660
cn18
Mef2dtm1Eno/Mef2dtm1Eno
Tg(Myog-cre)1Eno/0
Not Specified MGI:4418150


Genotype
MGI:4418137
cn1
Allelic
Composition
Hdac4tm1Eno/Hdac4tm2.1Eno
Hdac5tm1Eno/Hdac5tm1Eno
Tg(Myog-cre)1Eno/0
Genetic
Background
involves: 129 * 129S/SvEv * 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hdac4tm1Eno mutation (0 available); any Hdac4 mutation (112 available)
Hdac4tm2.1Eno mutation (0 available); any Hdac4 mutation (112 available)
Hdac5tm1Eno mutation (0 available); any Hdac5 mutation (57 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
muscle
• soleus muscles show an increase in the percentage of slow myofibers




Genotype
MGI:5576914
cn2
Allelic
Composition
Ppargc1atm2.1Brsp/Ppargc1atm2.1Brsp
Tg(Myog-cre)1Eno/0
Genetic
Background
involves: 129 * BALB/c * C57BL/6J * C57BL/6N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppargc1atm2.1Brsp mutation (1 available); any Ppargc1a mutation (48 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• at 3 and 12 months in fasting mice
• in the dark phase only
• in aged mice
• however, glucose tolerance is normal at 3 and 12 months
• in aged mice
• however, insulin resistance is normal at 6 months

growth/size/body
N
• mice exhibit normal body weight
• in aged mice

cellular
• decreased succinate dehydrogenase activity in the gastrocnemius of young and old mice

adipose tissue




Genotype
MGI:6476968
cn3
Allelic
Composition
Obscntm1Chen/Obscntm1Chen
Obsl1tm1.1Slan/Obsl1tm1.1Slan
Tg(Myog-cre)1Eno/0
Genetic
Background
involves: 129 * Black Swiss * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Obscntm1Chen mutation (1 available); any Obscn mutation (420 available)
Obsl1tm1.1Slan mutation (0 available); any Obsl1 mutation (100 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice are viable and develop normally

muscle
N
• analysis of myofilament structure using sarcomeric alpha-actinin 2 indicated normal sarcomerogenesis in tibialis anterior (TA) muscles
• immunofluorescence analysis of sarcomeric alpha-actinin 2 and titin-M8 localization revealed that Z-disc and M-band structures are not significantly altered
• at 4 months of age, muscle weight to tibia-length ratios for TA, soleus, gastrocnemius and extensor digitorum longus (EDL) muscles are normal
• no significant changes are observed in the number of centralized nuclei in TA muscle at 4 months of age
• skeletal muscles show a slight decrease in protein levels of utrophin and other dystrophin-sarcoglycan (DSG) components, including alpha-dystrobrevin, whereas levels of tubulin are slightly increased
• although overall dystrophin levels are normal, subsarcolemmal dystrophin localization in longitudinal sections of TA muscles is more patchy and abnormally distributed than in single Obscntm1Chen knockouts, indicating exacerbated membrane fragility
• a significant portion of TA muscle fibers are mouse IgG-positive, unlike in single Obscntm1Chen knockouts or Obsl1 skeletal muscle-knockouts, suggesting impaired sarcolemmal integrity
• increased membrane fragility leads to upregulation of dysferlin and filamin C proteins (involved in muscle repair), reduced caveolin-1 and TRPC1 protein levels, but normal levels of neuronal nitric oxidase (nNOS) and L-type calcium channel DHPR alpha-2 subunit, indicating potential changes to DSG-associated, but not T-tubule-based ion channels
• TA muscles show a decrease in small ankyrin-1.5 (sAnk1.5) protein levels similar to that in single Obscntm1Chen knockouts
• skeletal muscles show alterations to levels of lumenal SR calcium binding proteins (sarcalumenin and Casq2) as well as sarcoendoplasmic reticulum Ca2+ ATPase (Serca)
• proteome and expression data revealed increases in junctional SR proteins like triadin, junction and ryanodine receptors
• analysis of cross-sectional areas of TA muscle revealed a decrease in fiber size
• analysis of twitch parameters in EDL muscles revealed increased time-to-peak (TtP) values relative to control and Obsl1 skeletal muscle-knockouts
• however, half-relaxation times remain normal

homeostasis/metabolism
• monoamine oxidase A and B levels are significantly decreased in TA muscles
• catalase levels are significantly increased in soleus muscle
• muscle glycogen phosphorylase, the rate determining enzyme responsible for glycogen breakdown, is significantly decreased

cellular
• almost all identified mitochondrial electron transport chain proteins are downregulated in soleus and TA muscles
• analysis of whole TA and/or soleus muscle extracts using oxphos antibody cocktail or a Uqcrb antibody revealed slightly or significantly reduced levels of mitochondrial complex I, II, III, IV, and V proteins

reproductive system
N
• mice are fertile




Genotype
MGI:6476965
cn4
Allelic
Composition
Obsl1tm1.1Slan/Obsl1tm1.1Slan
Tg(Myog-cre)1Eno/0
Genetic
Background
involves: 129 * Black Swiss * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Obsl1tm1.1Slan mutation (0 available); any Obsl1 mutation (100 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice do not exhibit premature death or gross morphological abnormalities

muscle
N
• mice exhibit normal sarcomerogenesis in tibialis anterior (TA) muscles; Z-disc and M-band structures are not significantly altered
• no significant changes are observed in the number of centralized nuclei in TA muscle at 4 months of age
• at 4 months of age, muscle weight to tibia-length ratio is slightly increased for extensor digitorum longus (EDL) muscles
• however, muscle weight to tibia-length ratios for TA, soleus, and gastrocnemius are normal
• analysis of cross-sectional areas in TA muscles revealed an increase in fiber size

limbs/digits/tail
• at 4 months of age, muscle weight to tibia-length ratio is slightly increased for extensor digitorum longus (EDL) muscles
• however, muscle weight to tibia-length ratios for TA, soleus, and gastrocnemius are normal




Genotype
MGI:5576900
cn5
Allelic
Composition
Ppargc1atm2Brsp/Ppargc1a+
Tg(Myog-cre)1Eno/0
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppargc1atm2Brsp mutation (0 available); any Ppargc1a mutation (48 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• mice fed a high fat diet exhibit normal heat production and oxygen consumption
• in mice fed a high fat diet
• however, mice fed standard chow exhibit normal glucose serum levels
• in mice fed standard chow or a high fat diet

immune system

behavior/neurological
N
• mice fed a high fat diet exhibit normal food intake

growth/size/body
N
• mice fed standard chow or a high fat diet exhibit normal body weight and composition




Genotype
MGI:5575857
cn6
Allelic
Composition
Cygbtm1Ppam/Cygbtm1Ppam
Tg(Myog-cre)1Eno/0
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cygbtm1Ppam mutation (0 available); any Cygb mutation (17 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Delayed regeneration of muscle in Cygbtm1Ppam/Cygbtm1Ppam Tg(Myog-cre)1Eno/0 mice after cardiotoxin injury

muscle
• muscle progenitor cells are unable to differentiate fully in vitro
• full differentiation into myotubes is impaired in vitro
• prolonged muscle degeneration at 21 days after cardiotoxin-induced injury
• muscle progenitor cell proliferation is impaired in vitro
• 14 days postinjury induced by cardiotoxin

cellular
• increase both in duration and magnitude of myocyte death after cardiotoxin-induced injury
• muscle progenitor cells are unable to differentiate fully in vitro
• full differentiation into myotubes is impaired in vitro
• muscle progenitor cell proliferation is impaired in vitro
• in muscles at 21 days post cardiotoxin-induced injury




Genotype
MGI:5576899
cn7
Allelic
Composition
Ppargc1atm1Brsp/Ppargc1atm2Brsp
Tg(Myog-cre)1Eno/0
Genetic
Background
involves: 129 * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppargc1atm1Brsp mutation (1 available); any Ppargc1a mutation (48 available)
Ppargc1atm2Brsp mutation (0 available); any Ppargc1a mutation (48 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• mice fed standard chow or a high fat diet exhibit normal insulin tolerance
• hepatic glucose output under basal and clamped conditions is normal
• in mice fed a high fat diet
• in mice fed a high fat diet
• in mice fed a high fat diet
• mice exhibit increased systemic glucose uptake and glycolysis compared with control mice
• however, glycogen synthesis is normal
• in fed mice on standard chow
• however, fasted mice exhibit normal blood glucose levels
• in fasted and fed mice on a high fat diet
• in fed mice on standard chow or a high fat diet
• in fed mice on a high fat diet
• in mice fed a high fat diet

endocrine/exocrine glands
N
• islets exhibit normal basal and glucose-stimulated insulin secretion

growth/size/body
• in mice fed standard chow or a high fat diet
• in mice fed a high fat diet

immune system

adipose tissue
• in mice fed standard chow or a high fat diet

cellular
• decreased function as measured by Cox and succinate dehydrogenase activity

behavior/neurological
• during the day and night in mice fed a high fat diet




Genotype
MGI:3530886
cn8
Allelic
Composition
Srftm2.1Nor/Srftm2.1Nor
Tg(Myog-cre)1Eno/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Srftm2.1Nor mutation (0 available); any Srf mutation (27 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Curved spine and cyanosis in Srftm2.1Nor/Srftm2.1Nor Tg(Myog-cre)1Eno/0 mice

mortality/aging
• mutants die after birth from an inability to breathe

behavior/neurological
• mutants are immobile at birth

growth/size/body
• mutants weigh less at birth as a result of decreased muscle mass

homeostasis/metabolism

muscle
• muscle fibers are thinner than normal with large interstitial spaces however the normal number of nuclei are seen indicating a decrease in growth but not proliferation of the cells
• the sarcomere units are smaller and the fibers are narrow and disorganized
• abnormalities in the diaphragm muscle prevent breathing

respiratory system
• neonates are unable to breathe

skeleton

cardiovascular system
N
• no cardiac abnormalities are seen and the heart is beating at birth




Genotype
MGI:5616749
cn9
Allelic
Composition
Mbnl1tm1Sws/Mbnl1tm1Sws
Mbnl2tm1Sws/Mbnl2tm1Sws
Tg(Myog-cre)1Eno/0
Genetic
Background
involves: 129S1/Sv * 129S1/SvImJ * C57BL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mbnl1tm1Sws mutation (2 available); any Mbnl1 mutation (39 available)
Mbnl2tm1Sws mutation (0 available); any Mbnl2 mutation (66 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body

behavior/neurological
• develop severe motor deficits beginning at 12 weeks of age

skeleton
• develop kyphosis beginning at 12 weeks of age

muscle
• profound deficiency of adult skeletal muscle, with severe muscle pathology including small myofibers, fiber size heterogeneity, and centralized nuclei in nearly all myofibers




Genotype
MGI:4450935
cn10
Allelic
Composition
Acacbtm1.1Lowl/Acacbtm1.1Lowl
Tg(Myog-cre)1Eno/0
Genetic
Background
involves: 129S4/SvJaeSor * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Acacbtm1.1Lowl mutation (1 available); any Acacb mutation (109 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• no effect on bodyweight, food intake, or body composition
• little effect on ambient glucose and insulin levels




Genotype
MGI:4415790
cn11
Allelic
Composition
Mapk14tm1Lex/Mapk14tm1Lex
Tg(Myog-cre)1Eno/0
Genetic
Background
involves: 129S5/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk14tm1Lex mutation (1 available); any Mapk14 mutation (43 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• mice exhibit normal angiogenesis in response to endurance exercise

cellular
N
• mice exhibit normal mitochondrial biogenesis in response to endurance exercise

muscle
N
• mice exhibit normal fiber-type transformation in response to endurance exercise




Genotype
MGI:5554580
cn12
Allelic
Composition
Pnpla2tm1Eek/Pnpla2tm1Eek
Tg(Myog-cre)1Eno/0
Genetic
Background
involves: 129S * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pnpla2tm1Eek mutation (1 available); any Pnpla2 mutation (33 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• increase in diacylglycerol levels (specifically subspecies C14:0/16:0, C14:0/18:0, C16:0/18:0) in skeletal muscle in mice fed both chow and high fat diet as compared to control
• increase in fatty acid-CoA levels (specifically subspecies C14:0, C16:0) in mice fed both chow and high fat diet as compared to controls
• increase in intramyocellular triacylglycerol (IMTG) levels in skeletal muscle; increase is specific to muscle fiber type (2A>2X>1, but not 2B)
• IMTG levels are increased in mice fed both chow and high fat diet as compared to controls

muscle
• increase in intramyocellular triacylglycerol (IMTG) levels in skeletal muscle; increase is specific to muscle fiber type (2A>2X>1, but not 2B)
• IMTG levels are increased in mice fed both chow and high fat diet as compared to controls




Genotype
MGI:4418186
cn13
Allelic
Composition
Hdac4tm2.1Eno/Hdac4tm2.1Eno
Tg(Myog-cre)1Eno/0
Genetic
Background
involves: 129S/SvEv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hdac4tm2.1Eno mutation (0 available); any Hdac4 mutation (112 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• reinnervation occurs more rapidly compared to controls after nerve crush or cut
• however, in the absence of injury no defects in neuromuscular junctions are detected




Genotype
MGI:4418148
cn14
Allelic
Composition
Mef2ctm1Eno/Mef2ctm2Eno
Tg(Myog-cre)1Eno/0
Genetic
Background
involves: 129S/SvEv * 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mef2ctm1Eno mutation (0 available); any Mef2c mutation (34 available)
Mef2ctm2Eno mutation (0 available); any Mef2c mutation (34 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
muscle
• reduction in slow fibers within the soleus
• loss of type I fibers in the gastrocnemius and plantaris muscles and a decrease in number and intensity of type I fibers in the soleus




Genotype
MGI:4415789
cn15
Allelic
Composition
Mapk12tm1Lex/Mapk12tm1Lex
Tg(Myog-cre)1Eno/0
Genetic
Background
involves: 129S/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk12tm1Lex mutation (1 available); any Mapk12 mutation (17 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• marker expression indicates that exercise-induced angiogenesis is decreased compared to in similarly treated wild-type mice

cellular
• marker expression indicates that exercise-induced mitochondrial biogenesis is decreased compared to in similarly treated wild-type mice

muscle
N
• mice exhibit normal fiber-type transformation in response to endurance exercise




Genotype
MGI:4415788
cn16
Allelic
Composition
Mapk11tm2Lex/Mapk11tm2Lex
Tg(Myog-cre)1Eno/0
Genetic
Background
involves: 129S/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk11tm2Lex mutation (1 available); any Mapk11 mutation (35 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• mice exhibit normal angiogenesis in response to endurance exercise

cellular
N
• mice exhibit normal mitochondrial biogenesis in response to endurance exercise

muscle
N
• mice exhibit normal fiber-type transformation in response to endurance exercise




Genotype
MGI:5471660
cn17
Allelic
Composition
Gnai2tm2.1Lbi/Gnai2tm2.1Lbi
Gnai3tm1Lbi/Gnai3tm1Lbi
Tg(Myog-cre)1Eno/0
Genetic
Background
involves: 129S/SvEv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gnai2tm2.1Lbi mutation (0 available); any Gnai2 mutation (56 available)
Gnai3tm1Lbi mutation (1 available); any Gnai3 mutation (28 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Rib fusion phenotype is enhanced in Gnai3tm1Lbi/Gnai3tm1Lbi mice by loss of Gnai2 in cartilage

skeleton
• rib fusions are similar in severity to mice homozygous for Gnai3tm1Lbi alone




Genotype
MGI:4418150
cn18
Allelic
Composition
Mef2dtm1Eno/Mef2dtm1Eno
Tg(Myog-cre)1Eno/0
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mef2dtm1Eno mutation (0 available); any Mef2d mutation (66 available)
Tg(Myog-cre)1Eno mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
muscle
• slow fibers within the soleus are reduced





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last database update
11/12/2024
MGI 6.24
The Jackson Laboratory