Overview

Also Known As:PGC-1alpha KO

Mice that are homozygous for this Ppargc1a (peroxisome proliferative activated receptor, gamma, coactivator 1 alpha) knock-out mutation exhibit some postnatal lethality, impaired mitochondrial function and gluconeogenesis, are hypermetabolic, hyperactive, and sensitive to cold temperatures. This mutant mouse strain may be useful in studies of metabolic homeostasis, resistance to obesity, hyperactivity and behavior, mitochondrial impairment and neurodegeneration, and heart failure.

Donating Investigator

Bruce M Spiegelman, Dana-Farber Cancer Institute/Harvard Medical School

Genetic overview

Genetic Background	Generation
	N10+N1F11 (2020-03-19 00:00:00)

Ppargc1a^tm1Brsp

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Ppargc1a	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha

View Genetics

Research Applications

Diabetes and Obesity Research
Cardiovascular Research
Metabolism Research
Developmental Biology Research
Research Tools
Neurobiology Research

View All Research Applications

Base Price

Starting at:

$255.00 Domestic price for female 4-week

333.51 Domestic price for breeder pair

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Details

Detailed Description

Mice that are homozygous for this targeted mutation are fertile, normal in size and do not display any gross physical or behavioral abnormalities. Approximately half of homozygotes exhibit postnatal lethality. The Donating Investigator reports maintaining homozygous pups at a higher temperature (77°F) increases their survival. No gene product (mRNA or protein) is detected by RNA hybridization, real-time PCR analysis of skeletal muscle or liver, or Western blot analysis of brown fat. Histological examination of the brown fat from homozygotes reveals abnormal accumulation of large lipid droplets. Examination of brain tissue shows spongiform lesions and gliosis. When fed a high fat diet homozygotes have increased insulin sensitivity, glucose tolerance and reduced body weight. After 24 hours of fasting, homozygotes develop mild hypoglycemia. Mutants have impaired mitochondrial function and gluconeogenesis and are hypermetabolic as well as hyperactive. Homozygotes are unable to survive exposure to 4°C for more than 6 hours. Exaggerated startle response, stimulus induced myoclonus, dystonic posturing, and limb clasping are also observed. Transverse aortic constriction (TAC) results in dilated cardiomyopathy and development of heart failure. The Donating Investigator reports that heterozygote X heterozygote crosses yields less than the expected Mendelian ratio (the observed ratio is 1 homozygote in 8); and homozygous mice are more likely to have litters disappear or die after birth. This mutant mouse strain may be useful in studies of metabolic homeostasis, resistance to obesity, hyperactivity and behavior, mitochondrial impairment, neurodegeneration, and heart failure.

Development

A loxP site flanked targeting vector containing hygromycin resistance and thymidine kinase genes utilized in the construction of this mutant. This selection cassette was inserted downstream of exon 5 of the targeted gene, and another loxP site was inserted upstream of exon 3. This construct was electroporated into 129S4/SvJae derived J1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into recipient blastocysts. The resulting chimeric animals were crossed to C57BL/6 mice. The resulting offspring were then crossed to transgenic mice (on the C57BL/6 genetic background) expressing Cre recombinase under the control of the zona pellucida 3 (Zp3) promoter to remove exons 3 through 5 and the selection cassette. Heterozygotes were crossed to generate homozygotes. The donating investigator reported that the mice were then backcrossed to C57BL/6 (see SNP note below) for 9 generations before arriving at The Jackson Laboratory.

A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, all 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice sent to The Jackson Laboratory Repository were on a C57BL/6N genetic background.

Control Suggestions

Wild-type from the colony

Approximate Controls

Additional Information

Considerations for Choosing Controls

Selected References

Lin J; Wu PH; Tarr PT; Lindenberg KS; St-Pierre J; Zhang CY; Mootha VK; Jager S; Vianna CR; Reznick RM; Cui L; Manieri M; Donovan MX; Wu Z; Cooper MP; Fan MC; Rohas LM; Zavacki AM; Cinti S; Shulman GI; Lowell BB; Krainc D; Spiegelman BM. 2004. Defects in adaptive energy metabolism with CNS-linked hyperactivity in PGC-1alpha null mice. Cell 119(1):121-35PubMed: 15454086 MGI: J:93896

View All References

Genetics

Ppargc1a^tm1Brsp

Allele Symbol: Ppargc1a^tm1Brsp

Allele Name	targeted mutation 1, Bruce M Spiegelman
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	PGC-1alpha^-
Gene Symbol and Name	Ppargc1a, peroxisome proliferative activated receptor, gamma, coactivator 1 alpha
Gene Synonym(s)
Strain of Origin	129S4/SvJae
Chromosome	5
Molecular Note	This allele resulted from the crossing of Ppargc1a^tm2Brsp with mice expressing cre recombinase in the germline. Exons 3-5 were removed from the locus. Northern and Western blot analyses indicated a lack of transcript and protein in mutants.
Mutations Made By	Bruce Spiegelman, Dana-Farber Cancer Institute/Harvard Medical School

Disease/Phenotype

Disease Terms

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

age related macular degeneration

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Diabetes and Obesity Research
- Hyperglycemia
  - diet-induced, moderate
Cardiovascular Research
- Other
- Heart Abnormalities
- Metabolic Syndrome
Metabolism Research
- Lipid Metabolism
Developmental Biology Research
- Embryonic Lethality (Homozygous)
  - incomplete
- Perinatal Lethality
  - Homozygous
Research Tools
- Diabetes and Obesity Research
Neurobiology Research
- Neurodegeneration
- Behavioral and Learning Defects

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Ppargc1a^tm1Brsp/Ppargc1a^tm1Brsp
involves: 129/Sv * C57BL/6 * FVB/N

adipose tissue phenotype

abnormal brown adipose tissue morphology
- abundant, large lipid droplets are seen in the brown fat

growth/size/body region phenotype

decreased susceptibility to diet-induced obesity
- on a high fat diet homozygous mutants are significantly leaner compared to wild-type mice

homeostasis/metabolism phenotype

abnormal gluconeogenesis
- conversion of pyruvate into glucose is reduced following intraperitoneal pyruvate injection

abnormal glucose homeostasis

abnormal lipid homeostasis

decreased circulating insulin level
- fed but not fasted mutants have decreased insulin levels relative to fed or fasted wild-type mice, respectively

decreased liver triglyceride level
- triglyceride levels are lower in the livers of fasted mutant mice

decreased susceptibility to diet-induced obesity
- on a high fat diet homozygous mutants are significantly leaner compared to wild-type mice

hypoglycemia
- fasted mutants develop mild hypoglycemia after 24 hours

impaired adaptive thermogenesis
- mutants are unable to maintain body temperature in response to cold temperatures developing lethal hypothermia when exposed to 4^oC for more than 6 hours

improved glucose tolerance
- on a high fat diet homozygous mutants have significantly increased glucose tolerance compared to wild-type mice

increased insulin sensitivity
- on a high fat diet homozygous mutants have significantly increased insulin sensitivity compared to wild-type mice

increased oxygen consumption
- on a high fat diet oxygen consumption is increased 23% compared to wild-type mice
- total oxygen consumption is increased 17% in primary hepaotcytes

behavior/neurological phenotype

anhedonia
- mice exhibit decreased sucrose consumption as compared to wild-type mice
- sucrose consumption is decreased further following administration of kynurenine (KYN)

dystonia
- dystonic posturing is seen

hyperactivity
- a 40% increase in the frequency of random movements is seen

increased startle reflex
- an exaggerated startle response is seen

limb grasping

myoclonus
- stimulus induced myoclonus is seen

liver/biliary system phenotype

decreased liver triglyceride level
- triglyceride levels are lower in the livers of fasted mutant mice

mortality/aging

increased sensitivity to induced morbidity/mortality
- homozygotes die when exposed to 4^oC for more than 6 hours

postnatal lethality, incomplete penetrance
- about 50% of homozygotes die during the postnatal period

muscle phenotype

dystonia
- dystonic posturing is seen

myoclonus
- stimulus induced myoclonus is seen

nervous system phenotype

abnormal neuron morphology
- striatal neurons with reduced branches of neurites and occasional vacuoles within the neurons are seen

gliosis
- gliosis is seen associated with the spongiform lesions

myoclonus
- stimulus induced myoclonus is seen

spongiform encephalopathy
- spongiform lesions are seen predominantly in the striatum and to a lesser extent in the cortex
- the lesions are mostly associated with the white matter

cellular phenotype

abnormal cellular respiration
- respiration due to mitochondrial proton leak is increased 20% in primary hepatocytes

Genotype: Ppargc1a^tm1Brsp/Ppargc1a⁺
involves: 129 * FVB/N

mammalian phenotype

immune system phenotype
- Normal - mice exhibit normal serum IL6 levels

Genotype: Ppargc1a^tm1Brsp/Ppargc1a^tm1Brsp
involves: 129 * FVB/N

cardiovascular system phenotype

congestive heart failure
- TAC leads to accelerated cardiac dysfunction, accompanied by signs of heart failure

increased heart weight
- hearts from mutants subjected to transverse aortic constriction are more increased in weight and dilated than wild-type

increased response of heart to induced stress
- 2 months after transverse aortic constriction (TAC), develop profound cardiac dysfunction, with hearts becoming dilated and showing impaired ability to contract

growth/size/body region phenotype

cachexia
- 2 months after TAC, mutants are visibly emaciated and show significant drops in weight, unlike wild-type

increased heart weight
- hearts from mutants subjected to transverse aortic constriction are more increased in weight and dilated than wild-type

increased lung weight
- lungs are nearly quadrupled in weight 2 months after TAC as compared with only a moderate increase in wild-type TAC mice

homeostasis/metabolism phenotype

increased response of heart to induced stress
- 2 months after transverse aortic constriction (TAC), develop profound cardiac dysfunction, with hearts becoming dilated and showing impaired ability to contract

immune system phenotype

increased interleukin-6 secretion
- in myotubes

respiratory system phenotype

increased lung weight
- lungs are nearly quadrupled in weight 2 months after TAC as compared with only a moderate increase in wild-type TAC mice

Genotype: Ppargc1a^tm1Brsp/Ppargc1a⁺
involves: 129S4/SvJae * C57BL/6

cardiovascular system phenotype

abnormal choriocapillaris morphology
- mice fed a high-fat diet show a greater loss of fenestration in choriocapillaris endothelium

abnormal choroid vasculature morphology
- mice fed a regular diet show enlarged blood vessels in the interface between the Bruch's membrane and the choroid, with congestion and dilatation of some vessels

nervous system phenotype

retinal photoreceptor degeneration
- mice fed a high-fat diet exhibit a thinner photoreceptor layer, indicating degeneration of this layer
- photoreceptor degeneration does not necessarily initiate concurrently in both eyes

short photoreceptor inner segment
- mice fed a regular diet and a high-fat diet show a reduction of thickness of the inner segment layer

short photoreceptor outer segment
- mice fed a regular diet and a high-fat diet show a reduction of thickness of the outer segment layer

pigmentation phenotype

abnormal melanosome transport
- mice fed a high-fat diet show scant melanosomes migrating into the outer segment

abnormal retinal pigment epithelium morphology
- mice fed a high-fat diet show a greater accumulation of lipofuscin in the cytoplasm of the RPE, basal laminar deposits, and thickening of the outer collagenous layer
- mice fed a high-fat diet show RPE retinal pigment epithelium degeneration, with disruptions or gaps and scant melanosomes in the subretinal space migrating into the outer segment
- mice fed a regular diet show higher numbers of lipofuscin deposits in the retinal pigment epithelium (RPE) than wild-type mice

lipofuscinosis
- mice fed a high-fat diet show a greater accumulation of lipofuscin in the cytoplasm of the RPE
- mice fed a regular diet show higher numbers of lipofuscin deposits than wild-type mice

vision/eye phenotype

abnormal Bruch membrane morphology
- mice fed a high-fat diet show accumulation of carboxymethyl lysine (CML) deposits in the thickened Bruch membrane, indicating oxidative damage
- mice fed a high-fat diet show changes in the Bruch membrane, either atrophy or thickening in various regions

abnormal choriocapillaris morphology
- mice fed a high-fat diet show a greater loss of fenestration in choriocapillaris endothelium

abnormal choroid vasculature morphology
- mice fed a regular diet show enlarged blood vessels in the interface between the Bruch's membrane and the choroid, with congestion and dilatation of some vessels

abnormal retinal pigment epithelium morphology
- mice fed a high-fat diet show a greater accumulation of lipofuscin in the cytoplasm of the RPE, basal laminar deposits, and thickening of the outer collagenous layer
- mice fed a high-fat diet show RPE retinal pigment epithelium degeneration, with disruptions or gaps and scant melanosomes in the subretinal space migrating into the outer segment
- mice fed a regular diet show higher numbers of lipofuscin deposits in the retinal pigment epithelium (RPE) than wild-type mice

retinal macular degeneration
- mice fed a high-fat diet present age-related macular degeneration-like abnormalities in the retinal pigment epithelium and retinal morphology and function

retinal photoreceptor degeneration
- mice fed a high-fat diet exhibit a thinner photoreceptor layer, indicating degeneration of this layer
- photoreceptor degeneration does not necessarily initiate concurrently in both eyes

short photoreceptor inner segment
- mice fed a regular diet and a high-fat diet show a reduction of thickness of the inner segment layer

short photoreceptor outer segment
- mice fed a regular diet and a high-fat diet show a reduction of thickness of the outer segment layer

cellular phenotype

abnormal mitochondrial physiology
- mice fed a high-fat diet show a greater decrease in mitochondrial complex I activity in the retinal pigment epithelium/retina

decreased mitochondrial DNA content
- mice fed a high-fat diet show a greater decrease in mtDNA copy number than wild-type mice

impaired autophagy
- autophagy is reduced in the retinal pigment epithelium/retina

oxidative stress
- mice fed a high-fat diet show accumulation of carboxymethyl lysine deposits in the thickened Bruchs membrane, indicating oxidative damage
- mice fed a high-fat diet show increased reactive oxygen species (ROS) levels in the retinal pigment epithelium/retina

homeostasis/metabolism phenotype

impaired autophagy
- autophagy is reduced in the retinal pigment epithelium/retina

immune system phenotype

increased inflammatory response
- lipopolysaccharide (LPS) injection induces a higher inflammatory response in the retinal pigment epithelium (RPE)/retina compared to in wild-type mice

References

Lin J; Wu PH; Tarr PT; Lindenberg KS; St-Pierre J; Zhang CY; Mootha VK; Jager S; Vianna CR; Reznick RM; Cui L; Manieri M; Donovan MX; Wu Z; Cooper MP; Fan MC; Rohas LM; Zavacki AM; Cinti S; Shulman GI; Lowell BB; Krainc D; Spiegelman BM. 2004. Defects in adaptive energy metabolism with CNS-linked hyperactivity in PGC-1alpha null mice. Cell 119(1):121-35PubMed: 15454086 MGI: J:93896

Additional - Ppargc1a^tm1Brsp related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Ppargc1a^tm1Brsp
- Standard PCR:Ppargc1a^tm1Brsp
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

When maintaining a live colony, these mice can be bred as homozygotes, however approximately 50% of homozygotes exhibit postnatal lethality. The Donating Investigator reports maintaining homozygous pups at a higher temperature (77°F) increases their survival; heterozygote X heterozygote crosses yields less than the expected Mendelian ratio (the observed ratio is 1 homozygote in 8); and homozygous mice are more likely to have litters disappear or die after birth.
- Additional Breeding and Husbandry Support
Mating System
- +/+ sibling x Heterozygote
Citation
When using the PGC-1alpha KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #008597 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX10 (Standard)

Pricing & Availability

Available

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International

Live Mouse

Age

Genotype

Price

weeks

Breeder Pair

Sex

Genotype

Price

Female
Male

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous or wild-type for Ppargc1a<tm1Brsp>

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Also Known As:PGC-1alpha KO

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

Ppargc1atm1Brsp

Allele Symbol: Ppargc1atm1Brsp

Disease Terms

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Mammalian Phenotype Terms by Genotype

Genotype: Ppargc1atm1Brsp/Ppargc1atm1Brspinvolves: 129/Sv * C57BL/6 * FVB/N

adipose tissue phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

behavior/neurological phenotype

liver/biliary system phenotype

mortality/aging

muscle phenotype

nervous system phenotype

cellular phenotype

Genotype: Ppargc1atm1Brsp/Ppargc1a+involves: 129 * FVB/N

mammalian phenotype

Genotype: Ppargc1atm1Brsp/Ppargc1atm1Brspinvolves: 129 * FVB/N

cardiovascular system phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

immune system phenotype

respiratory system phenotype

Genotype: Ppargc1atm1Brsp/Ppargc1a+involves: 129S4/SvJae * C57BL/6

cardiovascular system phenotype

nervous system phenotype

pigmentation phenotype

vision/eye phenotype

cellular phenotype

homeostasis/metabolism phenotype

immune system phenotype

References

Additional - Ppargc1atm1Brsp related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Citation

Animal Health Reports

Live Mouse

Breeder Pair

Cryorecovery - Pricing

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Ppargc1a^tm1Brsp

Allele Symbol: Ppargc1a^tm1Brsp

Genotype: Ppargc1a^tm1Brsp/Ppargc1a^tm1Brsp
involves: 129/Sv * C57BL/6 * FVB/N

Genotype: Ppargc1a^tm1Brsp/Ppargc1a⁺
involves: 129 * FVB/N

Genotype: Ppargc1a^tm1Brsp/Ppargc1a^tm1Brsp
involves: 129 * FVB/N

Genotype: Ppargc1a^tm1Brsp/Ppargc1a⁺
involves: 129S4/SvJae * C57BL/6

Additional - Ppargc1a^tm1Brsp related