Strain Name:

B6.129S7(Cg)-Polgtm1Tprol/J

Stock Number:

017341

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Availability:

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Use Restrictions Apply, see Terms of Use
The PolgD257A mutant allele has a D257A mutation in the N-terminal "proofreading" exonuclease domain of the DNA polymerase γ gene (Polg), rendering the expressed mutant protein devoid of polymerase proofreading function in mitochondria. These mitochondrial mutator mice may be useful for studying the accumulation of mtDNA mutations in apoptosis, impaired energy metabolism, aging, and age-related conditions/diseases.

Description

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Mating SystemInbred x Heterozygote         (Female x Male)   30-NOV-12
Mating SystemHeterozygote x Heterozygote         (Female x Male)   30-NOV-12
Specieslaboratory mouse
GenerationN16+pN1 (28-JUL-13)
Generation Definitions
 
Donating Investigator Tomas A Prolla,   University of Wisconsin-Madison

Description
The PolgD257A mutant allele has a mitochondrial DNA polymerase editing amino acid substitution, D257Am in the N-terminal "proofreading" exonuclease domain II of the DNA polymerase γ gene (Polg). The expressed mutant protein, Polg-D257A, lacks the polymerase proofreading function/mismatch repair mechanism in mitochondria (although mtDNA replication is not significantly altered). As such, homozygous PolgD257A mice exhibit ~2500-fold increased rate of mtDNA mutation compared to wild-type mice. The accumulation of mtDNA mutations leads to increased apoptosis (particularly in cells/tissues that are metabolically active or have rapid cellular turnover). Homozygous (PolgD257A/D257A) mice grossly demonstrate a premature aging phenotype beginning at ~nine months of age with alopecia, graying hair, impaired mobility and kyphosis, and die prematurely by ~13-15 months of age with severe anemia. Homozygous mice exhibit several age-related defects, including thymic involution, weight loss, testicular atrophy, and cardiac hypertrophy/dysfunction, as well as progressive loss of skeletal muscle (sarcopenia), bone mass, circulating red blood cells, hearing, and intestinal crypts. The testicular atrophy manifests around five months of age concurrent with depletion of spermatogonia. The cardiovascular phenotype includes macrocytic anemia with abnormal erythroid maturation and megaloblastic changes, as well as profound defects in lymphopoiesis (characteristics of human myelodysplastic syndromes). The hearing loss is attributed to cochlear hair cell degeneration (presbycusis), with onset around nine months of age. Histologically, increased apoptosis in PolgD257A/D257A tissues is observable by three months of age in the duodenum, liver, testes, and thymus. Heterozygous mice (PolgD257A/+) also have an increased mutation burden, but no gross observable age-related phenotype, fertility problems, or other abnormalities are reported.

When PolgD257A mice are bred with Ins2Akita mice (Stock No. 003548), the double mutant offspring may be useful in studying appetite and diabetes.

Development
To create the targeting vector, Dr. Tomas A. Prolla (University of Wisconsin, Madison) isolated a mouse DNA polymerase γ (Polg) DNA sequence and used site-directed mutagenesis to introduce an AC-->CT two-base substitution corresponding to positions 1054-1055 in exon 3. The targeting vector also had a loxP-flanked PGK-neo cassette inserted into intron 3. The point mutations create a D257A amino acid substitution in the conserved N-terminal "proofreading" exonuclease domain II of Polg. This targeting construct was electroporated into 129S7/SvEvBrd-Hprtb-m2-derived AB2.2 embryonic stem (ES) cells, and correctly targeted ES cells were injected into blastocysts. Chimeric males were bred to C57BL/6J females. The PolgAD257Aneo mice were then bred with CMV-Cre transgenic mice (on a mixed 129/ICR genetic background) to remove the floxed PGK-neo cassette. The resulting mice harboring the PolgAD257A allele (also called PolgD257A, Polgmut, or PolgA) were subsequently backcrossed 16 generations to C57BL/6J wildtype mice (and the CMV-Cre transgene was removed) prior to sending to The Jackson Laboratory Repository. Upon arrival, mice were bred to C57BL/6J inbred mice (Stock No. 000664) for at least one generation.

Control Information

  Control
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

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

Polgtm1Tprol/Polgtm1Tprol

        involves: 129S7/SvEvBrd * C57BL/6J * ICR
  • mortality/aging
  • premature aging
    • premature aging is seen at 9 months of age   (MGI Ref ID J:99764)
  • premature death
    • maximum and median life span are reduced to 460 and 416 days, respectively   (MGI Ref ID J:99764)
  • cellular phenotype
  • abnormal mitochondrial physiology
    • by 9 months, homozygotes display increased mitochondrial DNA damage in the stria vascularis of the cochlea relative to age-matched wild-type mice   (MGI Ref ID J:119971)
  • increased apoptosis
    • levels of cleaved caspase-3 and TUNEL staining are increased at 3 months of age in the duodenum, liver, testes, and thymus and levels of cleaved caspase-3 are increased in the skeletal muscle at 9 months of age   (MGI Ref ID J:99764)
    • however, no increase in oxidative stress or cellular senescence are found   (MGI Ref ID J:99764)
  • endocrine/exocrine gland phenotype
  • abnormal crypts of Lieberkuhn morphology
    • age related loss of intestinal crypts   (MGI Ref ID J:99764)
  • abnormal thymus involution
    • thymus size and weight are reduced at 3 months of age   (MGI Ref ID J:99764)
  • testicular atrophy
    • age related testicular atrophy begins at 5 months of age   (MGI Ref ID J:99764)
  • growth/size/body phenotype
  • weight loss
    • age-related weight loss   (MGI Ref ID J:99764)
  • hearing/vestibular/ear phenotype
  • cochlear hair cell degeneration
    • by 9 months, homozygotes display significantly greater loss of cochlear hair cells (esp. OHCs) in the basal turn of the cochlea relative to age-matched wild-type mice or 2-mo-old homozygotes   (MGI Ref ID J:119971)
    • cochlear outer hair cell degeneration
      • by 9 months, homozygotes display significant loss of OHCs in the basal cochlear turn relative to age-matched wild-type mice or 2-mo-old homozygotes   (MGI Ref ID J:119971)
  • increased or absent threshold for auditory brainstem response
    • at 9 months, homozygotes display marked elevation of ABR thresholds at 4, 8, and 16 kHz relative to wild-type mice   (MGI Ref ID J:99764)
  • increased susceptibility to age-related hearing loss   (MGI Ref ID J:99764)
    • by 9 months of age, homozygotes display significantly elevated ABR thresholds at all test frequencies (4, 8, and 16 kHz) relative to wild-type mice   (MGI Ref ID J:119971)
    • in contrast, no significant ABR threshold elevations are observed at 2 months of age   (MGI Ref ID J:119971)
  • stria vascularis degeneration
    • by 9 months, homozygotes exhibit strial degeneration, evidenced as vacuolar degeneration associated with mitochondrial damage   (MGI Ref ID J:119971)
  • nervous system phenotype
  • cochlear ganglion degeneration   (MGI Ref ID J:99764)
    • by 9 months, homozygotes display significantly greater loss of spiral ganglion neurons in the lower basal turn of the cochlea relative to age-matched wild-type mice or 2-mo-old homozygotes   (MGI Ref ID J:119971)
  • cochlear hair cell degeneration
    • by 9 months, homozygotes display significantly greater loss of cochlear hair cells (esp. OHCs) in the basal turn of the cochlea relative to age-matched wild-type mice or 2-mo-old homozygotes   (MGI Ref ID J:119971)
    • cochlear outer hair cell degeneration
      • by 9 months, homozygotes display significant loss of OHCs in the basal cochlear turn relative to age-matched wild-type mice or 2-mo-old homozygotes   (MGI Ref ID J:119971)
  • hematopoietic system phenotype
  • abnormal thymus involution
    • thymus size and weight are reduced at 3 months of age   (MGI Ref ID J:99764)
  • decreased erythrocyte cell number
    • age-related reduction in red blood cell numbers   (MGI Ref ID J:99764)
  • immune system phenotype
  • abnormal thymus involution
    • thymus size and weight are reduced at 3 months of age   (MGI Ref ID J:99764)
  • muscle phenotype
  • decreased skeletal muscle mass
    • age-related reduction in skeletal muscle mass seen by 9 months of age   (MGI Ref ID J:99764)
  • skeleton phenotype
  • kyphosis
    • age-related kyphosis   (MGI Ref ID J:99764)
  • osteoporosis
    • age-related reduction in bone mass is seen earlier compared to wild-type mice   (MGI Ref ID J:99764)
  • pigmentation phenotype
  • abnormal coat/hair pigmentation
    • premature graying   (MGI Ref ID J:99764)
  • reproductive system phenotype
  • testicular atrophy
    • age related testicular atrophy begins at 5 months of age   (MGI Ref ID J:99764)
  • digestive/alimentary phenotype
  • abnormal crypts of Lieberkuhn morphology
    • age related loss of intestinal crypts   (MGI Ref ID J:99764)
  • integument phenotype
  • abnormal coat/hair pigmentation
    • premature graying   (MGI Ref ID J:99764)
  • premature hair loss   (MGI Ref ID J:99764)
View Research Applications

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

Apoptosis Research
Endogenous Regulators

Cancer Research
Genes Regulating Growth and Proliferation
Tumor Suppressor Genes

Cardiovascular Research
Heart Abnormalities
Vascular Defects

Cell Biology Research
DNA Damage Response
Genes Regulating Growth and Proliferation
Signal Transduction
Transcriptional Regulation

Dermatology Research
Skin and Hair Texture Defects

Developmental Biology Research
Internal/Organ Defects
      Lymphoid Tissue Defects
Lymphoid Tissue Defects
      hematopoietic defects
Skin and Hair Texture Defects

Hematological Research
Anemia, Iron Deficiency and Transport Defects
      macrocytic

Immunology, Inflammation and Autoimmunity Research
Lymphoid Tissue Defects
      hematopoietic development

Internal/Organ Research
Lymphoid Tissue Defects
Thymus Defects

Neurobiology Research
Ataxia (Movement) Defects
Hearing Defects
      Age related hearing loss

Reproductive Biology Research
Developmental Defects Affecting Gonads
      males only
Fertility Defects
      males only

Research Tools
Apoptosis Research
Cardiovascular Research
Reproductive Biology Research
      male germ cells

Sensorineural Research
Hearing Defects
      Age related hearing loss

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Polgtm1Tprol
Allele Name targeted mutation 1, T A Prolla
Allele Type Targeted
Common Name(s) PolgA; Polgm; Polgmut; PolgAD257A;
Mutation Made By Tomas Prolla,   University of Wisconsin-Madison
Strain of Origin129S7/SvEvBrd-Hprt
Promoter Polg, polymerase (DNA directed), gamma, mouse, laboratory
Molecular Note A targeting construct was designed to introduce an AC to CT two-base substitution in positions 1054 and 1055, resulting in a critical residue substitution in the conserved exonuclease domain. [MGI Ref ID J:99764]

Genotyping

Genotyping Information

Genotyping Protocols

Polgtm1Tprol, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Chen ML; Logan TD; Hochberg ML; Shelat SG; Yu X; Wilding GE; Tan W; Kujoth GC; Prolla TA; Selak MA; Kundu M; Carroll M; Thompson JE. 2009. Erythroid dysplasia, megaloblastic anemia, and impaired lymphopoiesis arising from mitochondrial dysfunction. Blood 114(19):4045-53. [PubMed: 19734452]  [MGI Ref ID J:154187]

Fox R; Kim HS; Reddick RL; Kujoth GC; Prolla TA; Tsutsumi S; Wada Y; Smithies O; Maeda N. 2011. Mitochondrial DNA polymerase editing mutation, PolgD257A, reduces the diabetic phenotype of Akita male mice by suppressing appetite. Proc Natl Acad Sci U S A 108(21):8779-84. [PubMed: 21555558]  [MGI Ref ID J:171899]

Hiona A; Sanz A; Kujoth GC; Pamplona R; Seo AY; Hofer T; Someya S; Miyakawa T; Nakayama C; Samhan-Arias AK; Servais S; Barger JL; Portero-Otin M; Tanokura M; Prolla TA; Leeuwenburgh C. 2010. Mitochondrial DNA mutations induce mitochondrial dysfunction, apoptosis and sarcopenia in skeletal muscle of mitochondrial DNA mutator mice. PLoS One 5(7):e11468. [PubMed: 20628647]  [MGI Ref ID J:163116]

Kujoth GC; Hiona A; Pugh TD; Someya S; Panzer K; Wohlgemuth SE; Hofer T; Seo AY; Sullivan R; Jobling WA; Morrow JD; Van Remmen H; Sedivy JM; Yamasoba T; Tanokura M; Weindruch R; Leeuwenburgh C; Prolla TA. 2005. Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian aging. Science 309(5733):481-4. [PubMed: 16020738]  [MGI Ref ID J:99764]

Vermulst M; Bielas JH; Kujoth GC; Ladiges WC; Rabinovitch PS; Prolla TA; Loeb LA. 2007. Mitochondrial point mutations do not limit the natural lifespan of mice. Nat Genet 39(4):540-3. [PubMed: 17334366]  [MGI Ref ID J:141666]

Additional References

Polgtm1Tprol related

Chen H; Vermulst M; Wang YE; Chomyn A; Prolla TA; McCaffery JM; Chan DC. 2010. Mitochondrial fusion is required for mtDNA stability in skeletal muscle and tolerance of mtDNA mutations. Cell 141(2):280-9. [PubMed: 20403324]  [MGI Ref ID J:167952]

Dai DF; Johnson SC; Villarin JJ; Chin MT; Nieves-Cintron M; Chen T; Marcinek DJ; Dorn GW 2nd; Kang YJ; Prolla TA; Santana LF; Rabinovitch PS. 2011. Mitochondrial oxidative stress mediates angiotensin II-induced cardiac hypertrophy and Galphaq overexpression-induced heart failure. Circ Res 108(7):837-46. [PubMed: 21311045]  [MGI Ref ID J:183593]

Fox RG; Magness S; Kujoth GC; Prolla TA; Maeda N. 2012. Mitochondrial DNA polymerase editing mutation, PolgD257A, disturbs stem-progenitor cell cycling in the small intestine and restricts excess fat absorption. Am J Physiol Gastrointest Liver Physiol 302(9):G914-24. [PubMed: 22345551]  [MGI Ref ID J:187490]

Han C; Someya S. 2013. Mouse models of age-related mitochondrial neurosensory hearing loss. Mol Cell Neurosci 55:95-100. [PubMed: 22820179]  [MGI Ref ID J:203587]

Jang YC; Remmen VH. 2009. The mitochondrial theory of aging: insight from transgenic and knockout mouse models. Exp Gerontol 44(4):256-60. [PubMed: 19171187]  [MGI Ref ID J:146518]

Joseph AM; Adhihetty PJ; Wawrzyniak NR; Wohlgemuth SE; Picca A; Kujoth GC; Prolla TA; Leeuwenburgh C. 2013. Dysregulation of mitochondrial quality control processes contribute to sarcopenia in a mouse model of premature aging. PLoS One 8(7):e69327. [PubMed: 23935986]  [MGI Ref ID J:204458]

Safdar A; Bourgeois JM; Ogborn DI; Little JP; Hettinga BP; Akhtar M; Thompson JE; Melov S; Mocellin NJ; Kujoth GC; Prolla TA; Tarnopolsky MA. 2011. Endurance exercise rescues progeroid aging and induces systemic mitochondrial rejuvenation in mtDNA mutator mice. Proc Natl Acad Sci U S A 108(10):4135-40. [PubMed: 21368114]  [MGI Ref ID J:170832]

Someya S; Yamasoba T; Kujoth GC; Pugh TD; Weindruch R; Tanokura M; Prolla TA. 2008. The role of mtDNA mutations in the pathogenesis of age-related hearing loss in mice carrying a mutator DNA polymerase gamma. Neurobiol Aging 29(7):1080-92. [PubMed: 17363114]  [MGI Ref ID J:140916]

Yamasoba T; Someya S; Yamada C; Weindruch R; Prolla TA; Tanokura M. 2007. Role of mitochondrial dysfunction and mitochondrial DNA mutations in age-related hearing loss. Hear Res 226(1-2):185-93. [PubMed: 16870370]  [MGI Ref ID J:119971]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX18

Colony Maintenance

Breeding & HusbandryBoth heterozygous and homozygous mice have progressive accumulation of mtDNA point mutations. Considering that paternal mitochondrial DNA is actively eliminated following fertilization in mice, one can minimize the (undesirable) accumulation of these mutations in the germline by breeding wildtype females or C57BL/6J inbred females (Stock No. 000664) with heterozygous males.
Mating SystemInbred x Heterozygote         (Female x Male)   30-NOV-12
Heterozygote x Heterozygote         (Female x Male)   30-NOV-12

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $199.90Female or MaleHeterozygous for Polgtm1Tprol  
$199.90Female or MaleHomozygous for Polgtm1Tprol  
Price per Pair (US dollars $)Pair Genotype
$399.80Heterozygous for Polgtm1Tprol x Heterozygous for Polgtm1Tprol  
$271.90Wild-type for Polgtm1Tprol x Heterozygous for Polgtm1Tprol  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $259.90Female or MaleHeterozygous for Polgtm1Tprol  
$259.90Female or MaleHomozygous for Polgtm1Tprol  
Price per Pair (US dollars $)Pair Genotype
$519.80Heterozygous for Polgtm1Tprol x Heterozygous for Polgtm1Tprol  
$353.50Wild-type for Polgtm1Tprol x Heterozygous for Polgtm1Tprol  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Control Information

  Control
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
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