muscle
• soleus muscles show an increase in the percentage of slow myofibers
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Allele Symbol Allele Name Allele ID |
Tg(Myog-cre)1Eno transgene insertion 1, Eric N Olson MGI:3530558 |
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Summary |
18 genotypes
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• soleus muscles show an increase in the percentage of slow myofibers
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• at 3 and 12 months in fasting mice
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• at 3 and 24 months
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• in the dark phase only
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• in aged mice
• however, glucose tolerance is normal at 3 and 12 months
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• in aged mice
• however, insulin resistance is normal at 6 months
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N |
• mice exhibit normal body weight
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• in aged mice
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• decreased succinate dehydrogenase activity in the gastrocnemius of young and old mice
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• in aged mice
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
N |
• mice are viable and develop normally
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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
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• 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
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• 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
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• analysis of cross-sectional areas of TA muscle revealed a decrease in fiber size
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• 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
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• monoamine oxidase A and B levels are significantly decreased in TA muscles
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• catalase levels are significantly increased in soleus muscle
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• muscle glycogen phosphorylase, the rate determining enzyme responsible for glycogen breakdown, is significantly decreased
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• 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
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N |
• mice are fertile
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
N |
• mice do not exhibit premature death or gross morphological abnormalities
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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
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• 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
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• analysis of cross-sectional areas in TA muscles revealed an increase in fiber size
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• 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
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
N |
• mice fed a high fat diet exhibit normal heat production and oxygen consumption
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• in mice fed a high fat diet
• however, mice fed standard chow exhibit normal glucose serum levels
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• in mice fed standard chow or a high fat diet
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N |
• mice fed a high fat diet exhibit normal food intake
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N |
• mice fed standard chow or a high fat diet exhibit normal body weight and composition
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♀ | 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 progenitor cells are unable to differentiate fully in vitro
• full differentiation into myotubes is impaired in vitro
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• prolonged muscle degeneration at 21 days after cardiotoxin-induced injury
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• muscle progenitor cell proliferation is impaired in vitro
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• 14 days postinjury induced by cardiotoxin
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• increase both in duration and magnitude of myocyte death after cardiotoxin-induced injury
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• muscle progenitor cells are unable to differentiate fully in vitro
• full differentiation into myotubes is impaired in vitro
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• muscle progenitor cell proliferation is impaired in vitro
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• in muscles at 21 days post cardiotoxin-induced injury
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
N |
• mice fed standard chow or a high fat diet exhibit normal insulin tolerance
• hepatic glucose output under basal and clamped conditions is normal
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• in mice fed a high fat diet
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• in mice fed a high fat diet
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• in mice fed a high fat diet
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• mice exhibit increased systemic glucose uptake and glycolysis compared with control mice
• however, glycogen synthesis is normal
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• in fed mice on standard chow
• however, fasted mice exhibit normal blood glucose levels
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• in fasted and fed mice on a high fat diet
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• in fed mice on standard chow or a high fat diet
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• in fed mice on a high fat diet
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• in mice fed a high fat diet
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N |
• islets exhibit normal basal and glucose-stimulated insulin secretion
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• reduced cell size
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• in mice fed standard chow or a high fat diet
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• in mice fed a high fat diet
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• in mice fed standard chow or a high fat diet
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• decreased function as measured by Cox and succinate dehydrogenase activity
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• during the day and night in mice fed a high fat diet
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• mutants die after birth from an inability to breathe
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• mutants are immobile at birth
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• mutants weigh less at birth as a result of decreased muscle mass
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• 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
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• abnormalities in the diaphragm muscle prevent breathing
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• neonates are unable to breathe
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N |
• no cardiac abnormalities are seen and the heart is beating at birth
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• develop severe motor deficits beginning at 12 weeks of age
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• profound deficiency of adult skeletal muscle, with severe muscle pathology including small myofibers, fiber size heterogeneity, and centralized nuclei in nearly all myofibers
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• no effect on bodyweight, food intake, or body composition
• little effect on ambient glucose and insulin levels
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
N |
• mice exhibit normal angiogenesis in response to endurance exercise
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N |
• mice exhibit normal mitochondrial biogenesis in response to endurance exercise
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N |
• mice exhibit normal fiber-type transformation in response to endurance exercise
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• 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
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• 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
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• 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
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• 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
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• 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
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• 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
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• marker expression indicates that exercise-induced angiogenesis is decreased compared to in similarly treated wild-type mice
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• marker expression indicates that exercise-induced mitochondrial biogenesis is decreased compared to in similarly treated wild-type mice
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N |
• mice exhibit normal fiber-type transformation in response to endurance exercise
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
N |
• mice exhibit normal angiogenesis in response to endurance exercise
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N |
• mice exhibit normal mitochondrial biogenesis in response to endurance exercise
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N |
• mice exhibit normal fiber-type transformation in response to endurance exercise
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• rib fusions are similar in severity to mice homozygous for Gnai3tm1Lbi alone
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• slow fibers within the soleus are reduced
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 11/12/2024 MGI 6.24 |
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