Description

Strain Information

Type Coisogenic; Mutant Strain; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Mating System Heterozygote x +/+ sibling         (Female x Male)   01-OCT-11 Mating System +/+ sibling x Heterozygote         (Female x Male)   27-DEC-11 Species laboratory mouse Background Strain 129S1/SvImJ Generation N27+ (27-DEC-11) Generation Definitions   Donating Investigator Leslie P. Kozak,   Pennington BioMedical Research Center

Description
Mice that are homozygous for this knockout allele are viable and fertile, but exhibit sensitivity to cold temperatures. The Donating Investigator notes that homozygous offspring have increased survival rates to weaning age when maintained at 25°C to 28°C. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brown adipose tissue from homozygotes. When maintained at 20°C, homozygotes are resistant to diet induced obesity with reduced white fat depot weights, exhibit a 0.1-0.3°C higher body temperature, and a slightly lowered respiratory quotient compared to controls. Notably, when maintained at 27°C, homozygous mutant mice are no longer resistant to diet induced obesity and gain weight at a rate similar to wildtype controls. An increase in the number of brown adipocytes in the inguinal fat depots is observed in mutant mice maintained at 20°C, on either diet. Homozygotes have reduced levels of plasma fatty acids, circulating triglyceride levels, and T4 levels. Spleen cell numbers are reduced by approximately 3-fold, CD8 single positive cells are reduced to approximately half and CD4/CD8 double positive cells in both the spleen and thymus are increased in homozygous animals. Homozygotes have no heat production from brown adipose tissue. Mitochondria isolated from the muscles of cold-acclimated homozygotes display an increased total ATP production capacity, a metabolic shift for increased lipid oxidation and reduced carbohydrate catabolism capacity with a corresponding increased serum level of beta-hydroxybuterate, and decreased sensitivity to fatty acids as uncoupling agents. Mitochondria isolated from brown adipose tissue from homozygotes exhibit increased rate of reactive oxygen species (ROS) production when compared to wildtype controls. The Donating Investigator reports that mice carrying this allele are less cold sensitive on the C57BL/6 genetic background compared to the 129 genetic background.

Development
A targeting vector was used to replace a BamHI/BglII fragment carrying exon 2 and part of exon 3 with the neo^r gene thereby deleting an essential membrane-spanning domain. The construct was electroporated into 129S2/SvPas derived D3 embryonic stem (ES) cells. Correctly targeted ES cells were injected into recipient blastocysts. The resulting chimeric animals were crossed to 129Sv/ImJ mice, and then backcrossed to 129Sv/ImJ for 25 generations. Upon arrival at The Jackson Laboratory, the mice were crossed to 129S1/SvImJ (Stock No. 002448) at least once to establish the colony.

Control Information

	Control
	Wild-type from the colony
	002448 129S1/SvImJ
Considerations for Choosing Controls

Related Strains

Strains carrying   Ucp1^tm1Kz allele

003124

B6.129-Ucp1tm1Kz/J

View Strains carrying   Ucp1^tm1Kz     (1 strain)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI

- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested. Obesity   (UCP1)

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI

      assigned by genotype

Ucp1^tm1Kz/Ucp1^tm1Kz

        involves: 129S2/SvPas

• adipose tissue phenotype
• increased brown adipose tissue amount
  • mass of brown fat was greater in homozygous mice than in controls; thought to be due to increased deposition of triglyceride   (MGI Ref ID J:40053)
• homeostasis/metabolism phenotype
• abnormal oxygen consumption
  • reduced oxygen consumption compared to controls was observed after treatment with a beta3-adrenergic agonist; resting oxygen consuption levels were similar to controls   (MGI Ref ID J:40053)
• • decreased oxygen consumption
    • in CL316243-treated mice   (MGI Ref ID J:62312)
• abnormal physiological response to xenobiotic
  • abnormal response to beta3-adrenergic stimulation by the CL 316,243 agonist   (MGI Ref ID J:40053)
• decreased susceptibility to diet-induced obesity
  • animals did not become obese on either a low-fat or a high-fat diet   (MGI Ref ID J:40053)
  • no changes were observed in the body mass, selected fat-pad mass or in total body triglyceride content   (MGI Ref ID J:40053)
  • normal food intake was observed   (MGI Ref ID J:40053)
• impaired adaptive thermogenesis
  • increased sensitivity to cold temperatures; most homozygous mice could not sustain body temperature when exposed to cold   (MGI Ref ID J:40053)
• growth/size phenotype
• decreased susceptibility to diet-induced obesity
  • animals did not become obese on either a low-fat or a high-fat diet   (MGI Ref ID J:40053)
  • no changes were observed in the body mass, selected fat-pad mass or in total body triglyceride content   (MGI Ref ID J:40053)
  • normal food intake was observed   (MGI Ref ID J:40053)

Ucp1^tm1Kz/Ucp1^tm1Kz

        129S1.Cg-Ucp^tm1Kz

• adipose tissue phenotype
• increased brown adipose tissue amount
  • increased brown adipose tissue depot weight   (MGI Ref ID J:69573)
• cellular phenotype
• abnormal mitochondrial physiology
  • mitochondria exhibit an impaired response to free fatty acid-induced decoupling to a de-energized state; linoleic acid, lauric acid and stearic acid stimulation of mitochondria showed reduced rates of de-energization compared to controls as measured by protonmotive force and oxygen consumption   (MGI Ref ID J:69573)
  • comparable content of mitochondrial protein   (MGI Ref ID J:69573)
  • decreased cytochrome c oxidase activity   (MGI Ref ID J:69573)
  • increased mitochondrial glycerol-3-phosphate dehydrogenase activity   (MGI Ref ID J:69573)
• homeostasis/metabolism phenotype
• impaired adaptive thermogenesis
  • lost body core temperature rapidly upon exposure to cold temperatures   (MGI Ref ID J:69573)

The following phenotype information may relate to a genetic background differing from this JAX^® Mice strain.

Ucp1^tm1Kz/Ucp1^tm1Kz

        B6.Cg-Ucp^tm1Kz

• adipose tissue phenotype
• decreased white adipose tissue amount
  • reduced weight of all white fat depots after a high-fat diet and exposure to 20^oC temperatures for 8 weeks   (MGI Ref ID J:81820)
• increased brown adipose tissue amount
  • an increase in the number of brown adipocytes in the inguinal fat pad was observed at at 20^oC on a high-fat diet   (MGI Ref ID J:81820)
• cellular phenotype
• abnormal mitochondrial physiology
  • mitochondria exhibit an impaired response to free fatty acid-induced decoupling to a de-energized state; linoleic acid, lauric acid and stearic acid stimulation of mitochondria showed reduced rates of de-energization compared to controls as measured by protonmotive force and oxygen consumption   (MGI Ref ID J:69573)
• growth/size phenotype
• decreased body weight
  • temperature dependent; at 20^oC, animals did not gain weight as quickly as controls on a high-fat, high-sucrose diet, but at 27^oC, the differences in body weight between mutants and controls were indistiguishable   (MGI Ref ID J:81820)
  • both groups of animals consumed similar amounts of food, indicating that the differences in body weight was not due to differences in energy intake   (MGI Ref ID J:81820)
• decreased susceptibility to diet-induced obesity
  • at 20^oC on a high-fat diet   (MGI Ref ID J:81820)
• homeostasis/metabolism phenotype
• abnormal lipid homeostasis
  • blood levels of beta-hydroxybuterate were significantly higher in homozygous mice suggesting higher fat oxidation rates   (MGI Ref ID J:81820)
• • decreased circulating free fatty acid level
    • mice have reduced levels of plasma fatty acids relative to littermates at 20^oC   (MGI Ref ID J:81820)
  • decreased circulating triglyceride level
    • reduced levels in bloob   (MGI Ref ID J:81820)
• decreased circulating thyroxine level
  • T4 leves were decreased   (MGI Ref ID J:81820)
• decreased respiratory quotient
  • at 20^oC, the respiratory quotient (the ratio of the volume of CO2 produced to the volume of O2 consumed) is slightly reduced   (MGI Ref ID J:81820)
• decreased susceptibility to diet-induced obesity
  • at 20^oC on a high-fat diet   (MGI Ref ID J:81820)
• impaired adaptive thermogenesis
  • lost body core temperature rapidly upon exposure to cold temperatures   (MGI Ref ID J:69573)
• increased body temperature
  • 0.1-0.3^oC higher than controls   (MGI Ref ID J:81820)
• increased circulating triiodothyronine level
  • T3 levels were increased   (MGI Ref ID J:81820)

Ucp1^tm1Kz/Ucp1^tm1Kz

        involves: 129S2/SvPas * C57BL/6J

• cellular phenotype
• abnormal mitochondrial physiology
  • mutant mitochondria have lost the high GDP-binding capacity and do not become energized in reposnse to it; instead, mutant mitochondria are in a perpetually energized state   (MGI Ref ID J:57998)
  • mitochondria do respond to free fatty acids by uncoupling to a de-energized state similar to controls   (MGI Ref ID J:57998)

Ucp1^tm1Kz/Ucp1^tm1Kz

        (129S1.Cg-Ucp^tm1Kz x B6.Cg-Ucp^tm1Kz)F1

• cellular phenotype
• abnormal mitochondrial physiology
  • mitochondria exhibit an impaired response to free fatty acid-induced decoupling to a de-energized state; linoleic acid, lauric acid and stearic acid stimulation of mitochondria showed reduced rates of de-energization compared to controls as measured by protonmotive force and oxygen consumption   (MGI Ref ID J:69573)
• homeostasis/metabolism phenotype
• *normal* homeostasis/metabolism phenotype
  • maintained normal body temperature upon exposure to cold   (MGI Ref ID J:69573)

View Research Applications

Research Applications

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

Cardiovascular Research
Other
      altered fat metabolism

Diabetes and Obesity Research
Obesity Without Diabetes
      diet-induced, resistant

Endocrine Deficiency Research
Adipose Defects

Internal/Organ Research
Adipose Defects

Metabolism Research
Free Radical Research
Lipid Metabolism

Research Tools
Diabetes and Obesity Research
Metabolism Research

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol		Ucp1tm1Kz
Allele Name		targeted mutation 1, Leslie Kozak
Allele Type		Targeted (knock-out)
Common Name(s)		Ucp1-; Ucptm1;
Mutation Made By		Leslie Kozak,   Pennington BioMedical Research Center
Strain of Origin		129S2/SvPas
ES Cell Line Name		D3
ES Cell Line Strain		129S2/SvPas
Gene Symbol and Name		Ucp1, uncoupling protein 1 (mitochondrial, proton carrier)
Chromosome		8
Gene Common Name(s)		AI385626; SLC25A7; UCP; Ucpa; Uncp; expressed sequence AI385626;
Molecular Note		All of exon 2 and a portion of exon 3 were replaced by a neomycin selection cassette. The deleted region encoded an essential transmembrane domain. Transcript was undetected in homozygous mutant mice via Northern blot analysis. Western blot analysis confirmed the absence of encoded protein. [MGI Ref ID J:40053]

Genotyping

Genotyping Information

Genotyping Protocols

Ucp1^tm1Kzalternate2 MCA,

Separated MCA

Ucp1^tm1Kzalternate1 MCA,

Separated MCA

Ucp1^tm1Kzalternate1, Separated PCR
Ucp1^tm1Kzalternate2, Separated PCR

Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Enerback S; Jacobsson A; Simpson EM; Guerra C; Yamashita H; Harper ME ; Kozak LP. 1997. Mice lacking mitochondrial uncoupling protein are cold-sensitive but not obese [see comments] Nature 387(6628):90-4. [PubMed: 9139827]  [MGI Ref ID J:40053]

Additional References

Ucp1^tm1Kz related

Adams AE; Kelly OM; Porter RK. 2010. Absence of mitochondrial uncoupling protein 1 affects apoptosis in thymocytes, thymocyte/T-cell profile and peripheral T-cell number. Biochim Biophys Acta 1797(6-7):807-16. [PubMed: 20417612]  [MGI Ref ID J:165366]

Anunciado-Koza R; Ukropec J; Koza RA; Kozak LP. 2008. Inactivation of UCP1 and the glycerol phosphate cycle synergistically increases energy expenditure to resist diet-induced obesity. J Biol Chem 283(41):27688-97. [PubMed: 18678870]  [MGI Ref ID J:142314]

Bruton JD; Aydin J; Yamada T; Shabalina IG; Ivarsson N; Zhang SJ; Wada M; Tavi P; Nedergaard J; Katz A; Westerblad H. 2010. Increased fatigue resistance linked to Ca2+-stimulated mitochondrial biogenesis in muscle fibres of cold-acclimated mice. J Physiol 588(Pt 21):4275-88. [PubMed: 20837639]  [MGI Ref ID J:179545]

Clarke KJ; Adams AE; Manzke LH; Pearson TW; Borchers CH; Porter RK. 2012. A role for ubiquitinylation and the cytosolic proteasome in turnover of mitochondrial uncoupling protein 1 (UCP1). Biochim Biophys Acta 1817(10):1759-67. [PubMed: 22531154]  [MGI Ref ID J:188078]

Dlaskova A; Clarke KJ; Porter RK. 2010. The role of UCP 1 in production of reactive oxygen species by mitochondria isolated from brown adipose tissue. Biochim Biophys Acta 1797(8):1470-6. [PubMed: 20416274]  [MGI Ref ID J:165368]

Fedorenko A; Lishko PV; Kirichok Y. 2012. Mechanism of Fatty-Acid-Dependent UCP1 Uncoupling in Brown Fat Mitochondria. Cell 151(2):400-13. [PubMed: 23063128]  [MGI Ref ID J:189069]

Feldmann HM ; Golozoubova V ; Cannon B ; Nedergaard J. 2009. UCP1 ablation induces obesity and abolishes diet-induced thermogenesis in mice exempt from thermal stress by living at thermoneutrality. Cell Metab 9(2):203-9. [PubMed: 19187776]  [MGI Ref ID J:146646]

Fredriksson JM; Nikami H; Nedergaard J. 2005. Cold-induced expression of the VEGF gene in brown adipose tissue is independent of thermogenic oxygen consumption. FEBS Lett 579(25):5680-4. [PubMed: 16219308]  [MGI Ref ID J:102385]

Golozoubova V; Cannon B; Nedergaard J. 2006. UCP1 is essential for adaptive adrenergic nonshivering thermogenesis. Am J Physiol Endocrinol Metab 291(2):E350-7. [PubMed: 16595854]  [MGI Ref ID J:111348]

Gong DW; Monemdjou S; Gavrilova O; Leon LR; Marcus-Samuels B; Chou CJ; Everett C; Kozak LP; Li C; Deng C; Harper ME; Reitman ML. 2000. Lack of obesity and normal response to fasting and thyroid hormone in mice lacking uncoupling protein-3. J Biol Chem 275(21):16251-7. [PubMed: 10748195]  [MGI Ref ID J:62312]

Hofmann WE; Liu X; Bearden CM; Harper ME; Kozak LP. 2001. Effects of genetic background on thermoregulation and fatty acid-induced uncoupling of mitochondria in UCP1-deficient mice. J Biol Chem 276(15):12460-5. [PubMed: 11279075]  [MGI Ref ID J:69573]

Hutchinson DS; Chernogubova E; Dallner OS; Cannon B; Bengtsson T. 2005. Beta-adrenoceptors, but not alpha-adrenoceptors, stimulate AMP-activated protein kinase in brown adipocytes independently of uncoupling protein-1. Diabetologia 48(11):2386-95. [PubMed: 16160864]  [MGI Ref ID J:104710]

Inokuma K; Ogura-Okamatsu Y; Toda C; Kimura K; Yamashita H; Saito M. 2005. Uncoupling protein 1 is necessary for norepinephrine-induced glucose utilization in brown adipose tissue. Diabetes 54(5):1385-91. [PubMed: 15855324]  [MGI Ref ID J:105197]

Inokuma K; Okamatsu-Ogura Y; Omachi A; Matsushita Y; Kimura K; Yamashita H; Saito M. 2006. Indispensable role of mitochondrial UCP1 for antiobesity effect of beta3-adrenergic stimulation. Am J Physiol Endocrinol Metab 290(5):E1014-21. [PubMed: 16368788]  [MGI Ref ID J:108376]

Kusudo T; Kontani Y; Kataoka N; Ando F; Shimokata H; Yamashita H. 2011. Fatty acid-binding protein 3 stimulates glucose uptake by facilitating AS160 phosphorylation in mouse muscle cells. Genes Cells 16(6):681-91. [PubMed: 21501347]  [MGI Ref ID J:186948]

Liu X; Rossmeisl M; McClaine J; Kozak LP. 2003. Paradoxical resistance to diet-induced obesity in UCP1-deficient mice. J Clin Invest 111(3):399-407. [PubMed: 12569166]  [MGI Ref ID J:81820]

Matthias A; Jacobsson A; Cannon B; Nedergaard J. 1999. The bioenergetics of brown fat mitochondria from UCP1-ablated mice. Ucp1 is not involved in fatty acid-induced de-energization (uncoupling). J Biol Chem 274(40):28150-60. [PubMed: 10497167]  [MGI Ref ID J:57998]

McDaneld TG; Nielsen MK; Miner JL. 2002. Uncoupling proteins and energy expenditure in mice divergently selected for heat loss. J Anim Sci 80(3):602-8. [PubMed: 11890396]  [MGI Ref ID J:103289]

Meyer CW; Willershauser M; Jastroch M; Rourke BC; Fromme T; Oelkrug R; Heldmaier G; Klingenspor M. 2010. Adaptive thermogenesis and thermal conductance in wild-type and UCP1-KO mice. Am J Physiol Regul Integr Comp Physiol 299(5):R1396-406. [PubMed: 20826705]  [MGI Ref ID J:165580]

Monemdjou S; Hofmann WE; Kozak LP; Harper ME. 2000. Increased mitochondrial proton leak in skeletal muscle mitochondria of UCP1-deficient mice Am J Physiol Endocrinol Metab 279(4):E941-6. [PubMed: 11001779]  [MGI Ref ID J:65221]

Nolan MA; Sikorski MA; McKnight GS. 2004. The Role of Uncoupling Protein 1 in the Metabolism and Adiposity of RII{beta}-Protein Kinase A-Deficient Mice. Mol Endocrinol 18(9):2302-2311. [PubMed: 15192081]  [MGI Ref ID J:92076]

Oelkrug R; Kutschke M; Meyer CW; Heldmaier G; Jastroch M. 2010. Uncoupling protein 1 decreases superoxide production in brown adipose tissue mitochondria. J Biol Chem 285(29):21961-8. [PubMed: 20466728]  [MGI Ref ID J:165318]

Okamatsu-Ogura Y; Kitao N; Kimura K; Saito M. 2007. Brown fat UCP1 is not involved in the febrile and thermogenic responses to IL-1beta in mice. Am J Physiol Endocrinol Metab 292(4):E1135-9. [PubMed: 17164436]  [MGI Ref ID J:120398]

Shabalina I; Wiklund C; Bengtsson T; Jacobsson A; Cannon B; Nedergaard J. 2002. Uncoupling protein-1: involvement in a novel pathway for beta-adrenergic, cAMP-mediated intestinal relaxation. Am J Physiol Gastrointest Liver Physiol 283(5):G1107-16. [PubMed: 12381524]  [MGI Ref ID J:108275]

Shabalina IG; Backlund EC; Bar-Tana J; Cannon B; Nedergaard J. 2008. Within brown-fat cells, UCP1-mediated fatty acid-induced uncoupling is independent of fatty acid metabolism. Biochim Biophys Acta 1777(7-8):642-50. [PubMed: 18489899]  [MGI Ref ID J:136945]

Shabalina IG; Hoeks J; Kramarova TV; Schrauwen P; Cannon B; Nedergaard J. 2010. Cold tolerance of UCP1-ablated mice: A skeletal muscle mitochondria switch toward lipid oxidation with marked UCP3 up-regulation not associated with increased basal, fatty acid- or ROS-induced uncoupling or enhanced GDP effects. Biochim Biophys Acta 1797(6-7):968-80. [PubMed: 20227385]  [MGI Ref ID J:165382]

Shabalina IG; Jacobsson A; Cannon B; Nedergaard J. 2004. Native UCP1 displays simple competitive kinetics between the regulators purine nucleotides and fatty acids. J Biol Chem 279(37):38236-48. [PubMed: 15208325]  [MGI Ref ID J:92814]

Shabalina IG; Kramarova TV; Nedergaard J; Cannon B. 2006. Carboxyatractyloside effects on brown-fat mitochondria imply that the adenine nucleotide translocator isoforms ANT1 and ANT2 may be responsible for basal and fatty-acid-induced uncoupling respectively. Biochem J 399(3):405-14. [PubMed: 16831128]  [MGI Ref ID J:116035]

Shabalina IG; Petrovic N; Kramarova TV; Hoeks J; Cannon B; Nedergaard J. 2006. UCP1 and defense against oxidative stress. 4-Hydroxy-2-nonenal effects on brown fat mitochondria are uncoupling protein 1-independent. J Biol Chem 281(20):13882-93. [PubMed: 16543238]  [MGI Ref ID J:113503]

Ukropec J; Anunciado RP; Ravussin Y; Hulver MW; Kozak LP. 2006. UCP1-independent thermogenesis in white adipose tissue of cold-acclimated Ucp1-/- mice. J Biol Chem 281(42):31894-908. [PubMed: 16914547]  [MGI Ref ID J:117273]

Ukropec J; Anunciado RV; Ravussin Y; Kozak LP. 2006. Leptin is required for uncoupling protein-1-independent thermogenesis during cold stress. Endocrinology 147(5):2468-80. [PubMed: 16469807]  [MGI Ref ID J:129662]

Xue Y; Petrovic N; Cao R; Larsson O; Lim S; Chen S; Feldmann HM; Liang Z; Zhu Z; Nedergaard J; Cannon B; Cao Y. 2009. Hypoxia-independent angiogenesis in adipose tissues during cold acclimation. Cell Metab 9(1):99-109. [PubMed: 19117550]  [MGI Ref ID J:144343]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX18

Colony Maintenance

Breeding & Husbandry	When maintaining a live colony, these mice can be bred as heterozygotes. Although homozygotes are viable and fertile, they exhibit increased sensitivity to cold temperatures. The Donating Investigator notes that there is better survival of homozygous to weaning age when mice are maintained at 25°C to 28°C.
Mating System	Heterozygote x +/+ sibling         (Female x Male)   01-OCT-11
	+/+ sibling x Heterozygote         (Female x Male)   27-DEC-11
Diet Information	LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls

Control Information

	Control
	Wild-type from the colony
	002448 129S1/SvImJ
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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