Overview

Also Known As:Polg^A , Polg^m , Polg^mut, PolgA^D257A

The Polg^D257A 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.

Donating Investigator

Tomas A Prolla, University of Wisconsin-Madison

Genetic overview

Genetic Background	Generation
	N16p+N11 (2019-12-06 00:00:00)

Polg^tm1Prol

Allele Type	Gene Symbol	Gene Name
Targeted (Not Specified)	Polg	polymerase (DNA directed), gamma

View Genetics

Research Applications

Research Tools
Apoptosis Research
Reproductive Biology Research
Neurobiology Research
Sensorineural Research
Cancer Research
Cell Biology Research
Cardiovascular Research

View All Research Applications

Base Price

Starting at:

$255.00 Domestic price for female 4-week

281.05 Domestic price for breeder pair

View Price List

Details

Detailed Description

The Polg^D257A 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 Polg^D257A 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 (Polg^D257A/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 Polg^D257A/D257A tissues is observable by three months of age in the duodenum, liver, testes, and thymus.

Heterozygous mice (Polg^D257A/+) also have an increased mutation burden, but no gross observable age-related phenotype, fertility problems, or other abnormalities are reported.

When Polg^D257A mice are bred with Ins2^Akita 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-Hprt^b-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 PolgA^D257Aneo 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 PolgA^D257A allele (also called Polg^D257A, Polg^mut, or Polg^A) 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 Suggestions

Wild-type from the colony
000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

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):4045-53PubMed: 19734452 MGI: 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):8779-84PubMed: 21555558 MGI: 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):e11468PubMed: 20628647 MGI: 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):481-4PubMed: 16020738 MGI: 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):540-3PubMed: 17334366 MGI: J:141666

View All References

Genetics

Polg^tm1Prol

Allele Symbol: Polg^tm1Prol

Allele Name	targeted mutation 1, Tomas A Prolla
Allele Type	Targeted (Not Specified)
Allele Synonym(s)	mtDNA-mutator; Polg^A; Polg^m; Polg^mut; Polg^tm1Tprol; PolgA^D257A
Gene Symbol and Name	Polg, polymerase (DNA directed), gamma
Gene Synonym(s)
Promoter	Polg, polymerase (DNA directed), gamma, mouse, laboratory
Strain of Origin	129S7/SvEvBrd-Hprt^b-m2
Chromosome	7
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 (D257A).
Mutations Made By	Tomas Prolla, University of Wisconsin-Madison

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

myelodysplastic syndrome

Research Areas By Phenotype

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

Research Tools
- Apoptosis Research
- Reproductive Biology Research
  - male germ cells
- Cardiovascular Research
Apoptosis Research
- Endogenous Regulators
Reproductive Biology Research
- Fertility Defects
  - males only
- Developmental Defects Affecting Gonads
  - males only
Neurobiology Research
- Hearing Defects
  - Age related hearing loss
- Ataxia (Movement) Defects
Sensorineural Research
- Hearing Defects
  - Age related hearing loss
Cancer Research
- Genes Regulating Growth and Proliferation
- Tumor Suppressor Genes
Cell Biology Research
- Genes Regulating Growth and Proliferation
- Transcriptional Regulation
- DNA Damage Response
- Signal Transduction
Cardiovascular Research
- Vascular Defects
- Heart Abnormalities
Developmental Biology Research
- Internal/Organ Defects
  - Lymphoid Tissue Defects
- Lymphoid Tissue Defects
  - hematopoietic defects
- Skin and Hair Texture Defects
Immunology, Inflammation and Autoimmunity Research
- Lymphoid Tissue Defects
  - hematopoietic development
Internal/Organ Research
- Lymphoid Tissue Defects
- Thymus Defects
Dermatology Research
- Skin and Hair Texture Defects
Hematological Research
- Anemia, Iron Deficiency and Transport Defects
  - macrocytic

Mammalian Phenotype Terms by Genotype

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

Genotype: Polg^tm1Prol/Polg^tm1Prol
involves: 129S7/SvEvBrd * C57BL/6J * ICR

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

increased apoptosis
- however, no increase in oxidative stress or cellular senescence are found
- 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

hematopoietic system phenotype

abnormal thymus involution
- thymus size and weight are reduced at 3 months of age

decreased erythrocyte cell number
- age-related reduction in red blood cell numbers

immune system phenotype

abnormal thymus involution
- thymus size and weight are reduced at 3 months of age

integument phenotype

abnormal coat/hair pigmentation
- premature graying

premature hair loss

mortality/aging

premature aging
- premature aging is seen at 9 months of age

premature death
- maximum and median life span are reduced to 460 and 416 days, respectively

muscle phenotype

decreased skeletal muscle mass
- age-related reduction in skeletal muscle mass seen by 9 months of age

nervous system phenotype

cochlear ganglion degeneration
- 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

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

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

pigmentation phenotype

abnormal coat/hair pigmentation
- premature graying

reproductive system phenotype

testicular atrophy
- age related testicular atrophy begins at 5 months of age

skeleton phenotype

kyphosis
- age-related kyphosis

osteoporosis
- age-related reduction in bone mass is seen earlier compared to wild-type mice

digestive/alimentary phenotype

abnormal crypts of Lieberkuhn morphology
- age related loss of intestinal crypts

endocrine/exocrine gland phenotype

abnormal crypts of Lieberkuhn morphology
- age related loss of intestinal crypts

abnormal thymus involution
- thymus size and weight are reduced at 3 months of age

testicular atrophy
- age related testicular atrophy begins at 5 months of age

growth/size/body region phenotype

weight loss
- age-related weight loss

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

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

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

increased susceptibility to age-related hearing loss
- 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
- Normal - in contrast, no significant ABR threshold elevations are observed at 2 months of age

stria vascularis degeneration
- by 9 months, homozygotes exhibit strial degeneration, evidenced as vacuolar degeneration associated with mitochondrial damage

The following phenotype relates to a compound genotype created using this strain

Genotype: Polg^tm1Prol/Polg^tm1Prol
B6J.129S7-Polg

cellular phenotype

abnormal mitochondrial physiology
- as early as 4 months of age, a decreased cytochrome oxidase/citrate synthase ratio is seen in mitochondria of the spleen and this ratio is decreased in both spleen and liver mitochondria at 9-10 months of age, indicating mitochondrial dysfunction

endocrine/exocrine gland phenotype

decreased thymocyte number
- decrease in total viable thymocytes in 8-13 month old mice

immune system phenotype

abnormal lymphopoiesis
- abnormal lymphoid development in aging mice

decreased double-positive T cell number
- decrease in the relative frequency of CD4/CD8 double-positive cells in 8-13 month old mice

decreased immature B cell number
- 8-13 month old mice show defects in the generation of immature B/pre-B cells

decreased lymphocyte cell number
- Normal - however, mice do not develop leukocytosis or signs of leukemic conversion
- mice become lymphopenic by 8 months of age, involving both major lymphoid lineages

decreased mature B cell number
- bone marrow of 8-13 month old mice shows a decrease in mature B cells

decreased pre-B cell number
- 8-13 month old mice show defects in the generation of immature B/pre-B cells

decreased pro-B cell number
- 8-13 month old mice show defects in the generation of pro-B cells

decreased thymocyte number
- decrease in total viable thymocytes in 8-13 month old mice

hematopoietic system phenotype

abnormal erythroid lineage cell morphology
- 10 month old splenocytes exhibit stress erythropoiesis, with a significant increase in frequency of polychromatophilic normoblasts
- 8 month old mice exhibit an increase in the frequency of Ter119+ splenocytes, with a significant expansion in both polychromatophilic normoblasts and reticulocytes
- abnormal erythroid development in aging mice
- in the bone marrow of 10 month old mice, an expansion of polychormatophilic normoblasts is seen at the expense of both reticulocytes and mature red blood cells

abnormal lymphopoiesis
- abnormal lymphoid development in aging mice

decreased double-positive T cell number
- decrease in the relative frequency of CD4/CD8 double-positive cells in 8-13 month old mice

decreased hemoglobin content
- from 6 to 10 months of age, hemoglobin levels are moderately decreased and from 11 months onward, hemoglobin levels rapidly decrease

decreased immature B cell number
- 8-13 month old mice show defects in the generation of immature B/pre-B cells

decreased lymphocyte cell number
- Normal - however, mice do not develop leukocytosis or signs of leukemic conversion
- mice become lymphopenic by 8 months of age, involving both major lymphoid lineages

decreased mature B cell number
- bone marrow of 8-13 month old mice shows a decrease in mature B cells

decreased pre-B cell number
- 8-13 month old mice show defects in the generation of immature B/pre-B cells

decreased pro-B cell number
- 8-13 month old mice show defects in the generation of pro-B cells

decreased thymocyte number
- decrease in total viable thymocytes in 8-13 month old mice

increased erythroblast number
- 8 and 10 month old splenocytes and 10 month old bone marrow show an increase in the frequency of polychromatophilic normoblasts
- a population of erythroblasts characterized by intermediate cell size and low-to-negative expression of CD71 is expanded in the bone marrow of 10 month old mice; this population of orthochromic erythroblasts has abundant, fully hemoglobinized cytoplasm, indicating megoblastic morphologic changes
- ndicating megoblastic morphologic changes

increased mean corpuscular volume
- mean corpuscular volume of reticulocytes increases sharply from 8 months of age

macrocytic anemia
- macrocytic anemia appears as early as 6 months of age and progressively worsens
- transplantation of mutant marrow into wild-type recipients recapitulates age-related macrocytic anemia, lymphopenia, and megaloblastic changes

macrocytosis
- macrocytosis becomes evident after 8 months of age, shortly after development of anemia, and worsens with age

mortality/aging

premature death
- mice die by 15 months of age

References

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):4045-53PubMed: 19734452 MGI: 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):8779-84PubMed: 21555558 MGI: 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):e11468PubMed: 20628647 MGI: 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):481-4PubMed: 16020738 MGI: 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):540-3PubMed: 17334366 MGI: J:141666

Additional - Polg^tm1Prol related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Polg Alternate 1
- Genotyping resources and troubleshooting
Breeding Considerations

Both 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. The preferred method of generating homozygous mice with only a single generation of mutation burden would be to breed a heterozygous female (that originated from a wildtype/C57BL/6J female x heterozygous male cross) with a carrier male.

For the live colony at The Jackson Laboratory, we maintain a primary colony by breeding C57BL/6J females with heterozygous males - from which [i] some offspring are used for the next generation of primary colony breeding (C57BL/6J female x heterozygous male) and [ii] some heterozygous offspring are bred together as a secondary colony. Heterozygous mice from the primary colony are made available for distribution. The homozygous offspring from the secondary colony are made available for distribution. No additional breeding from the secondary colony is performed. Researchers interested in the availability of heterozygous offspring from the secondary colony may inquire with JAX Mice & Services Customer Support.
- Additional Breeding and Husbandry Support
Mating System
- C57BL/6J (000664) x Heterozygote
- Heterozygote x Heterozygote
Citation
When using the PolgA^D257A mouse strain in a publication, please cite the originating article(s) and include JAX stock #017341 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX12 (Maximum)

Pricing & Availability

Available

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Breeder Pair

Sex

Genotype

Price

Female
Male

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous or wildtype for Polg<tm1Tprol>

Related Products and Services

Frozen Mouse Embryo	B6.129S7(Cg)-Polg<tm1Prol>/J	$2595.00
Frozen Mouse Embryo	B6.129S7(Cg)-Polg<tm1Prol>/J	$2595.00
Frozen Mouse Embryo	B6.129S7(Cg)-Polg<tm1Prol>/J	$3373.50
Frozen Mouse Embryo	B6.129S7(Cg)-Polg<tm1Prol>/J	$3373.50

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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. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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Also Known As:PolgA , Polgm , Polgmut, PolgAD257A

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Polgtm1Prol

Allele Symbol: Polgtm1Prol

Disease Terms

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

Research Areas By Phenotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Polgtm1Prol/Polgtm1Prolinvolves: 129S7/SvEvBrd * C57BL/6J * ICR

cellular phenotype

hematopoietic system phenotype

immune system phenotype

integument phenotype

mortality/aging

muscle phenotype

nervous system phenotype

pigmentation phenotype

reproductive system phenotype

skeleton phenotype

digestive/alimentary phenotype

endocrine/exocrine gland phenotype

growth/size/body region phenotype

hearing/vestibular/ear phenotype

Genotype: Polgtm1Prol/Polgtm1ProlB6J.129S7-Polg

cellular phenotype

endocrine/exocrine gland phenotype

immune system phenotype

hematopoietic system phenotype

mortality/aging

References

Additional - Polgtm1Prol related

Genotyping Protocols

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

Additional Use Restrictions Apply

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Also Known As:Polg^A , Polg^m , Polg^mut, PolgA^D257A

Polg^tm1Prol

Allele Symbol: Polg^tm1Prol

Genotype: Polg^tm1Prol/Polg^tm1Prol
involves: 129S7/SvEvBrd * C57BL/6J * ICR

Genotype: Polg^tm1Prol/Polg^tm1Prol
B6J.129S7-Polg

Additional - Polg^tm1Prol related