| |||||||||||||||||||
| Mice that are homozygous for the targeted mutation exhibit a shortened circadian period and a loss of persistent circadian rhythmicity when maintained in constant darkness. This mutant mouse strain may be useful in studies related to the regulation of the sleep-wake cycle. | |||||||||||||||||||
- Description
- Disease & phenotype
- Genes & alleles
- Genotyping
- Health & care
- References
- Pricing & purchasing
- Terms of use
Description
Strain Information
Former Names B6.129S7-Per2tm1Brd/J (Changed: 27-APR-11 ) 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 System Homozygote x Homozygote (Female x Male) 01-MAR-06 Species laboratory mouse Generation N5F?+F24 (06-JAN-09)
Generation DefinitionsDonating Investigator Dr. Allan Bradley, Baylor College of Medicine Description
Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display gross physical or behavioral abnormalities. A mutant transcript, if translated, would generate a protein with an 87 amino acid deletion. When maintained in constant darkness, two phenotypic components are exhibited: a shortened circadian period and a loss of persistent circadian rhythmicity. When housed under constant light, homozygotes exhibit normal activity rhythm but a period length of less than 24 hours. By 9-12 months of age, homozygous females exhibit low reproductive success and produce small litters when compared to wildtype. These mice also carry the recessive Tyrc-Brd mutation that, when homozygous, results in albino coat color. This mutant mouse strain may be useful in studies related to the regulation of the sleep-wake cycle.Development
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt two Per2 exons encoding half of the PAS B domain and the entire PAC subdomain. The construct was transfected into 129S7/SvEvBrd-Hprtb-m2 derived AB2.2 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6-Tyrc-Brd blastocysts. The resulting chimeric mice were bred with C57BL/6-Tyrc-Brd mice (also called C57BL/6Brd-Tyrc-Brd). The donating investigator reported that mutant mice were then backcrossed to C57BL/6-Tyrc-Brd mice for at least five generations. Mice homozygous for both the Per2tm1Brd targeted mutation on chromosome 1 and the the recessive Tyrc-Brd mutation on chromosome 7 were sent to The Jackson Laboratory Repository (see SNP notes below).A 32 SNP (single nucleotide polymorphism) panel analysis, with markers covering all 19 chromosomes and the X chromosome, was performed on the rederived living colony at The Jackson Laboratory Repository. This revealed 3 markers (one on chromosome 1 and two on chromosome 15) that were not fixed for C57BL/6 allele-type. The marker on chromosome 1 appears to be fixed as homozygous for 129 allele-type. This marker is close to the Per2 locus and is likely to be original ES cell genome segregating with the Per2tm1Brd targeted mutation. The two markers on chromosome 15 (located at ~34 Mbp and ~58 Mbp) also appear to be fixed as homozygous for 129 allele-type. This may represent a large region of chromosome 15 that is fixed as homozygous for 129 allele-type.
Control Information
| Control | ||
|---|---|---|
| 000058 B6(Cg)-Tyrc-2J/J | ||
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying other alleles of Per2
010832 129S-Per2tm1Drw/J 016176 B6(Cg)-Tg(tetO-Per2)2Jt/J 010492 B6.129-Per2tm1Drw/J 006852 B6.129S6-Per2tm1Jt/J View Strains carrying other alleles of Per2 (4 strains)
Phenotype
Phenotype Information
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested. Advanced Sleep Phase Syndrome, Familial, 1; FASPS1 (PER2)
Albinism, Ocular, with Sensorineural Deafness (TYR)
Albinism, Oculocutaneous, Type IA; OCA1A (TYR)
Albinism, Oculocutaneous, Type IB; OCA1B (TYR)
assigned by genotype
Per2tm1Brd/Per2tm1Brd
involves: 129S7/SvEvBrd * C57BL/6
- mortality/aging
- early reproductive senescence
- mutant females exhibit accelerated reproductive ageing, as indicated by a higher incidence of irregular oestrous cycles and a lower reproductive success at 9-12 months of age (MGI Ref ID J:136165)
- increased mortality induced by gamma-irradiation
- gamma irradiated homozygotes exhibit premature hair greying and hair loss, and an increased rate of tumor formation (MGI Ref ID J:79456)
- at 22 weeks after irradiation, all homozygotes exhibit hair greying while 30% also show large areas of hair loss on the back or around neck and mouth (not found in any wild-type) (MGI Ref ID J:79456)
- at 7 months after irradiation, all mutant males display teratomas (not found in any wild-type) (MGI Ref ID J:79456)
- at 16 months after irradiation, all mutants with malignant lymphomas display severe morbidity (MGI Ref ID J:79456)
- premature death
- 30% of homozygotes die before the age of 16 months, with the first death noted at 9 months (MGI Ref ID J:79456)
- reproductive system phenotype
- abnormal male preputial gland morphology
- male mice months 18 months of age have enlarged preputial glands with severe duct ectasia, focal hyperplasia, and hyperkeratosis (MGI Ref ID J:79456)
- abnormal pregnancy
- unlike wild-type, middle-aged mutant females exhibit a significantly higher number of embryonic scars (implantations) in the uterus after two pregnancies than the total number of live offspring detected at birth or at weanining, suggesting post-implantation embryo loss due to insufficient energy levels (MGI Ref ID J:136165)
- absent estrous cycle
- middle-aged female mutants are acyclic for ~45% of a 6-week observation period, whereas age-matched wild-type females never show acyclicity (MGI Ref ID J:136165)
- decreased litter size
- mutiparous (second parturition) mutant females yield significantly smaller litter sizes than wild-type females (MGI Ref ID J:136165)
- middle-aged (9-12 months of age) female mutants produce significantly smaller litter sizes than young adult (2-6 months of age) wild-type or mutant females (MGI Ref ID J:136165)
- early reproductive senescence
- mutant females exhibit accelerated reproductive ageing, as indicated by a higher incidence of irregular oestrous cycles and a lower reproductive success at 9-12 months of age (MGI Ref ID J:136165)
- prolonged estrous cycle
- middle-aged female mutants display significantly less regular 4-day estrous and more prolonged cycles (>6 days) for ~55% of a 6-week observation period (MGI Ref ID J:136165)
- reduced female fertility
- primiparous (first parturition) mutant females fail to breed successfully whereas mutiparous (second parturition) mutant females yield significantly smaller litter sizes than wild-type females (MGI Ref ID J:136165)
- both primiparous and multiparous middle-aged (9-12 months of age) mutant females exhibit a lower reproductive success (either fewer litters or smaller litter sizes) than middle-aged wild-type females (MGI Ref ID J:136165)
- however, young adult mutant females (2-6 months of age) show the same success in fertility and fecundity as wild-type females (MGI Ref ID J:136165)
- behavior/neurological phenotype
- *normal* behavior/neurological phenotype
- abnormal food intake
- unlike pregnant wild-type females which show a progressive increase in food intake that correlates positively with body mass, middle-aged mutant females do not significantly increase their food intake during pregnancy (MGI Ref ID J:136165)
- whereas middle-aged wild-type females increase their food intake by 67.6% up to the 16th day of lactation, age-matched mutant females increase their food consumption by 40%; moreover, this increase fails to occur continuously as in wild-type females (MGI Ref ID J:136165)
- abnormal food preference
- unlike non-reproductive wild-type females which prefer 20% protein content, middle-aged non-reproductive mutant females do not display any preference to a certain protein content (MGI Ref ID J:136165)
- abnormal locomotor behavior
- homozygotes show elevated locomotor activity in a several-hour period preceding the light-to-dark transition (pre-dusk activity) (MGI Ref ID J:56167)
- abnormal maternal behavior
- unlike wild-type females, middle-aged mutant females spend an equal time in the nest during the three lactating stages (day 1, 11, and 21 of lactation) (MGI Ref ID J:136165)
- pup cannibalization
- all pups born to primiparous (first parturition) mutant females are cannibalised by their mothers (MGI Ref ID J:136165)
- abnormal sleep pattern
- homozygotes exhibit less NREM sleep and REM sleep than wild-type in the last 3 hours before dark onset (MGI Ref ID J:89417)
- homozygotes have more NREM sleep than wild-type in the first 2 hours after light onset (MGI Ref ID J:89417)
- at the light-dark transition, mutants initiate their waking episode earlier than wild-type, suggesting that the sleep/wake pattern is not masked by light (MGI Ref ID J:89417)
- notably, sleep homeostasis reflected by the slow-wave activity (SWA) increase after 6 hours of sleep deprivation is preserved (MGI Ref ID J:89417)
- addiction
- in response to acute i.p. cocaine injections (10 mg/kg), both wild-type and mutant mice display a similar (~5-fold) increase in locomotor activity from saline control levels (MGI Ref ID J:77340)
- however, after repeated cocaine administration, homozygotes show a hypersensitized behavioral response to cocaine relative to wild-type mice (MGI Ref ID J:77340)
- arrhythmic circadian persistence
- homozygotes exhibit loss of persistent circadian rhythmicity within 3 weeks in constant darkness (DD) (MGI Ref ID J:56167)
- most homozygotes do not lose their circadian rhythms immediately upon entry into DD (MGI Ref ID J:56167)
- upon loss of rhythmicity, a light pulse immediately restores their rhythms, indicating a partially functional clock (MGI Ref ID J:56167)
- enhanced conditioned place preference behavior
- homozygotes exhibit a pronounced preference to the cocaine-paired side in the conditioned place preference (CPP) paradigm; however, this response is not statistically different from that of wild-type mice (MGI Ref ID J:77340)
- shortened circadian period
- homozygotes entrain to the LD cycle (12 h light/12 h dark) but display a significantly shorter circadian period in constant darkness (MGI Ref ID J:56167)
- tumorigenesis
- increased incidence of ionizing radiation-induced tumors
- homozygotes exhibit a significantly higher frequency of tumor development than wild-type following gamma irradiation (MGI Ref ID J:79456)
- at 16 months after irradiation, 71% of irradiated mutants (versus only 5% of irradiated wild-type) develop malignant lymphomas in multiple organs (MGI Ref ID J:79456)
- increased lymphoma incidence
- 15% of homozygotes die of lymphoma before the age of 16 months (MGI Ref ID J:79456)
- skeleton phenotype
- abnormal bone ossification
- mice exhibit increased bone formation rate compared with wild-type mice (MGI Ref ID J:163112)
- increased bone volume
- at 3, 12, and 48 weeks, but not 24 weeks (MGI Ref ID J:163112)
- cellular phenotype
- decreased cellular sensitivity to gamma-irradiation
- mutant thymocytes exhibit a partial resistance to gamma radiation-induced apoptosis (MGI Ref ID J:79456)
- nervous system phenotype
- *normal* nervous system phenotype
- homozygotes show no anatomical defects in the suprachiasmatic nucleus of the anterior hypothalamus (MGI Ref ID J:56167)
- digestive/alimentary phenotype
- salivary gland epithelial hyperplasia
- renal/urinary system phenotype
- abnormal male preputial gland morphology
- male mice months 18 months of age have enlarged preputial glands with severe duct ectasia, focal hyperplasia, and hyperkeratosis (MGI Ref ID J:79456)
- growth/size phenotype
- abnormal body weight
- loss of body mass after parturition is less pronounced in middle-aged mutant females than in middle-aged wild-type females (MGI Ref ID J:136165)
- unlike lactating wild-type females, middle-aged mutant females show no significant changes in body mass over a 21-day lactation period (MGI Ref ID J:136165)
- increased body weight
- middle-aged mutant females are significantly heavier than wild-type females both during the non-reproductive and pregnant stages (MGI Ref ID J:136165)
- homeostasis/metabolism phenotype
- abnormal basal metabolism
- middle-aged mutant females exhibit a lower average daily metabolic rate than age-matched wild-type females both during the non-reproductive and reproductive (pregnancy and lactation) periods (MGI Ref ID J:136165)
- integument phenotype
- abnormal male preputial gland morphology
- male mice months 18 months of age have enlarged preputial glands with severe duct ectasia, focal hyperplasia, and hyperkeratosis (MGI Ref ID J:79456)
- endocrine/exocrine gland phenotype
- abnormal male preputial gland morphology
- male mice months 18 months of age have enlarged preputial glands with severe duct ectasia, focal hyperplasia, and hyperkeratosis (MGI Ref ID J:79456)
- salivary gland epithelial hyperplasia
This mouse can be used to support research in many areas including:
Per2tm1Brd relatedDermatology Research
Color and White Spotting Defects
skin and hair
Neurobiology Research
Circadian Rhythms
Cell Biology Research
Transcriptional Regulation
Endocrine Deficiency Research
Hypothalamus/Pituitary Defects
Neurobiology Research
Behavioral and Learning Defects
Circadian Rhythms
Genes & Alleles
Gene & Allele Information provided by MGI
| Allele Symbol | Per2tm1Brd | ||
|---|---|---|---|
| Allele Name | targeted mutation 1, Allan Bradley | ||
| Allele Type | Targeted (knock-out) | ||
| Common Name(s) | Per2Brdm1; mPer2Brdm1; mPer2m; | ||
| Mutation Made By | Dr. Allan Bradley, Baylor College of Medicine | ||
| Strain of Origin | 129S7/SvEvBrd-Hprt | ||
| ES Cell Line Name | AB2.2 | ||
| ES Cell Line Strain | 129S7/SvEvBrd-Hprt | ||
| Gene Symbol and Name | Per2, period circadian clock 2 | ||
| Chromosome | 1 | ||
| Gene Common Name(s) | FASPS; mKIAA0347; mPer2; rPER2; | ||
| Molecular Note | Two exons containing the most conserved region of the gene were replaced with PGK-neo cassette, resulting in the deletion of the PAC subdomain and half of the PAS B domain. RT-PCR and sequence analysis of mutant animals detected a mutant transcript with a predicted protein containing an 87 amino acid deletion. [MGI Ref ID J:56167] | ||
| Allele Symbol | Tyrc-Brd | ||
| Allele Name | albino, Allan Bradley | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | C57BL/6c-; cBrd; | ||
| Strain of Origin | C57BL/6 | ||
| Gene Symbol and Name | Tyr, tyrosinase | ||
| Chromosome | 7 | ||
| Gene Common Name(s) | C; CMM8; OCA1A; OCAIA; SHEP3; albino; c; skc35; skin/coat color 35; | ||
| Molecular Note | This mutation arose spontaneously in or around 1991 in the C57BL/6 colony of Dr. Alan Bradley. It has been used in linkage studies based on the location of the tyrosinase gene on Chr 7, and its phenotype is complemented by a tyrosinase mini-gene. Sequence analysis of exon 1 identified the same G-to-T transversion at nucleotide position 291 (G291T), resulting in replacement of arginine by leucine at amino acid position 77, that is present in the albino 2 Jackson allele. It reverts at a very low frequency (there were two incidences in the original colony between 1992 and 1995), resulting in black pups in otherwise albino litters. [MGI Ref ID J:115975] [MGI Ref ID J:115976] | ||
Genotyping
Genotyping Information
Genotyping Protocols
Per2tm1Brd, Separated PCR
Helpful Links
Genotyping resources and troubleshooting
References
References provided by MGI
Selected Reference(s)
Zheng B; Larkin DW; Albrecht U; Sun ZS; Sage M; Eichele G; Lee CC; Bradley A. 1999. The mPer2 gene encodes a functional component of the mammalian circadian clock. Nature 400(6740):169-73. [PubMed: 10408444] [MGI Ref ID J:56167]
Additional References
Fu L; Pelicano H; Liu J; Huang P; Lee C. 2002. The circadian gene period2 plays an important role in tumor suppression and DNA damage response in vivo. Cell 111(1):41. [PubMed: 12372299] [MGI Ref ID J:79456]
Zheng B; Albrecht U; Kaasik K; Sage M; Lu W; Vaishnav S; Li Q; Sun ZS; Eichele G; Bradley A; Lee CC. 2001. Nonredundant roles of the mPer1 and mPer2 genes in the mammalian circadian clock. Cell 105(5):683-94. [PubMed: 11389837] [MGI Ref ID J:69769]
Per2tm1Brd relatedTyrc-Brd relatedAbarca C; Albrecht U; Spanagel R. 2002. Cocaine sensitization and reward are under the influence of circadian genes and rhythm. Proc Natl Acad Sci U S A 99(13):9026-30. [PubMed: 12084940] [MGI Ref ID J:77340]
Carvas JM; Vukolic A; Yepuri G; Xiong Y; Popp K; Schmutz I; Chappuis S; Albrecht U; Ming XF; Montani JP; Yang Z. 2012. Period2 gene mutant mice show compromised insulin-mediated endothelial nitric oxide release and altered glucose homeostasis. Front Physiol 3:337. [PubMed: 22934083] [MGI Ref ID J:193434]
Cheng HY; Alvarez-Saavedra M; Dziema H; Choi YS; Li A; Obrietan K. 2009. Segregation of expression of mPeriod gene homologs in neurons and glia: possible divergent roles of mPeriod1 and mPeriod2 in the brain. Hum Mol Genet 18(16):3110-24. [PubMed: 19477955] [MGI Ref ID J:150729]
Eckle T; Hartmann K; Bonney S; Reithel S; Mittelbronn M; Walker LA; Lowes BD; Han J; Borchers CH; Buttrick PM; Kominsky DJ; Colgan SP; Eltzschig HK. 2012. Adora2b-elicited Per2 stabilization promotes a HIF-dependent metabolic switch crucial for myocardial adaptation to ischemia. Nat Med 18(5):774-82. [PubMed: 22504483] [MGI Ref ID J:183926]
Feillet CA; Mendoza J; Albrecht U; Pevet P; Challet E. 2008. Forebrain oscillators ticking with different clock hands. Mol Cell Neurosci 37(2):209-21. [PubMed: 17996461] [MGI Ref ID J:132601]
Feillet CA; Ripperger JA; Magnone MC; Dulloo A; Albrecht U; Challet E. 2006. Lack of food anticipation in Per2 mutant mice. Curr Biol 16(20):2016-22. [PubMed: 17055980] [MGI Ref ID J:116105]
Fu L; Patel MS; Bradley A; Wagner EF; Karsenty G. 2005. The molecular clock mediates leptin-regulated bone formation. Cell 122(5):803-15. [PubMed: 16143109] [MGI Ref ID J:115188]
Fu L; Pelicano H; Liu J; Huang P; Lee C. 2002. The circadian gene period2 plays an important role in tumor suppression and DNA damage response in vivo. Cell 111(1):41. [PubMed: 12372299] [MGI Ref ID J:79456]
Hampp G; Ripperger JA; Houben T; Schmutz I; Blex C; Perreau-Lenz S; Brunk I; Spanagel R; Ahnert-Hilger G; Meijer JH; Albrecht U. 2008. Regulation of monoamine oxidase a by circadian-clock components implies clock influence on mood. Curr Biol 18(9):678-83. [PubMed: 18439826] [MGI Ref ID J:135199]
Husse J; Hintze SC; Eichele G; Lehnert H; Oster H. 2012. Circadian clock genes Per1 and Per2 regulate the response of metabolism-associated transcripts to sleep disruption. PLoS One 7(12):e52983. [PubMed: 23285241] [MGI Ref ID J:195741]
Jeyaraj D; Scheer FA; Ripperger JA; Haldar SM; Lu Y; Prosdocimo DA; Eapen SJ; Eapen BL; Cui Y; Mahabeleshwar GH; Lee HG; Smith MA; Casadesus G; Mintz EM; Sun H; Wang Y; Ramsey KM; Bass J; Shea SA; Albrecht U; Jain MK. 2012. Klf15 orchestrates circadian nitrogen homeostasis. Cell Metab 15(3):311-23. [PubMed: 22405069] [MGI Ref ID J:182675]
Kaasik K; Lee CC. 2004. Reciprocal regulation of haem biosynthesis and the circadian clock in mammals. Nature 430(6998):467-71. [PubMed: 15269772] [MGI Ref ID J:91278]
Kopp C; Albrecht U; Zheng B; Tobler I. 2002. Homeostatic sleep regulation is preserved in mPer1 and mPer2 mutant mice. Eur J Neurosci 16(6):1099-106. [PubMed: 12383239] [MGI Ref ID J:89417]
Kowalska E; Ripperger JA; Hoegger DC; Bruegger P; Buch T; Birchler T; Mueller A; Albrecht U; Contaldo C; Brown SA. 2013. Feature Article: NONO couples the circadian clock to the cell cycle. Proc Natl Acad Sci U S A 110(5):1592-9. [PubMed: 23267082] [MGI Ref ID J:193286]
Lee S; Donehower LA; Herron AJ; Moore DD; Fu L. 2010. Disrupting circadian homeostasis of sympathetic signaling promotes tumor development in mice. PLoS One 5(6):e10995. [PubMed: 20539819] [MGI Ref ID J:161808]
Liu J; Mankani G; Shi X; Meyer M; Cunningham-Runddles S; Ma X; Sun ZS. 2006. The circadian clock Period 2 gene regulates gamma interferon production of NK cells in host response to lipopolysaccharide-induced endotoxic shock. Infect Immun 74(8):4750-6. [PubMed: 16861663] [MGI Ref ID J:112402]
Ma K; Xiao R; Tseng HT; Shan L; Fu L; Moore DD. 2009. Circadian dysregulation disrupts bile Acid homeostasis. PLoS One 4(8):e6843. [PubMed: 19718444] [MGI Ref ID J:152389]
Maronde E; Schilling AF; Seitz S; Schinke T; Schmutz I; van der Horst G; Amling M; Albrecht U. 2010. The clock genes Period 2 and Cryptochrome 2 differentially balance bone formation. PLoS One 5(7):e11527. [PubMed: 20634945] [MGI Ref ID J:163112]
Mendez-Ferrer S; Lucas D; Battista M; Frenette PS. 2008. Haematopoietic stem cell release is regulated by circadian oscillations. Nature 452(7186):442-7. [PubMed: 18256599] [MGI Ref ID J:134224]
Mendoza J; Albrecht U; Challet E. 2010. Behavioural food anticipation in clock genes deficient mice: confirming old phenotypes, describing new phenotypes. Genes Brain Behav 9(5):467-77. [PubMed: 20180860] [MGI Ref ID J:175063]
Meredith AL; Wiler SW; Miller BH; Takahashi JS; Fodor AA; Ruby NF; Aldrich RW. 2006. BK calcium-activated potassium channels regulate circadian behavioral rhythms and pacemaker output. Nat Neurosci 9(8):1041-1049. [PubMed: 16845385] [MGI Ref ID J:111722]
Miki T; Xu Z; Chen-Goodspeed M; Liu M; Van Oort-Jansen A; Rea MA; Zhao Z; Lee CC; Chang KS. 2012. PML regulates PER2 nuclear localization and circadian function. EMBO J 31(6):1427-39. [PubMed: 22274616] [MGI Ref ID J:181918]
Nakamura T; Takumi T; Takano A; Aoyagi N; Yoshiuchi K; Struzik ZR; Yamamoto Y. 2008. Of mice and men--universality and breakdown of behavioral organization. PLoS ONE 3(4):e2050. [PubMed: 18446212] [MGI Ref ID J:133642]
Oster H; Damerow S; Kiessling S; Jakubcakova V; Abraham D; Tian J; Hoffmann MW; Eichele G. 2006. The circadian rhythm of glucocorticoids is regulated by a gating mechanism residing in the adrenal cortical clock. Cell Metab 4(2):163-73. [PubMed: 16890544] [MGI Ref ID J:129730]
Oster H; Yasui A; Van Der Horst GT; Albrecht U. 2002. Disruption of mCry2 restores circadian rhythmicity in mPer2 mutant mice. Genes Dev 16(20):2633-8. [PubMed: 12381662] [MGI Ref ID J:79492]
Oster H; van der Horst GT; Albrecht U. 2003. Daily variation of clock output gene activation in behaviorally arrhythmic mPer/mCry triple mutant mice. Chronobiol Int 20(4):683-95. [PubMed: 12916720] [MGI Ref ID J:103060]
Owens L; Buhr E; Tu DC; Lamprecht TL; Lee J; Van Gelder RN. 2012. Effect of circadian clock gene mutations on nonvisual photoreception in the mouse. Invest Ophthalmol Vis Sci 53(1):454-60. [PubMed: 22159024] [MGI Ref ID J:191526]
Perreau-Lenz S; Zghoul T; de Fonseca FR; Spanagel R; Bilbao A. 2009. Circadian regulation of central ethanol sensitivity by the mPer2 gene. Addict Biol 14(3):253-9. [PubMed: 19523042] [MGI Ref ID J:165763]
Pilorz V; Steinlechner S. 2008. Low reproductive success in Per1 and Per2 mutant mouse females due to accelerated ageing? Reproduction 135(4):559-68. [PubMed: 18367514] [MGI Ref ID J:136165]
Preitner N; Damiola F; Lopez-Molina L; Zakany J; Duboule D; Albrecht U; Schibler U. 2002. The orphan nuclear receptor REV-ERBalpha controls circadian transcription within the positive limb of the mammalian circadian oscillator. Cell 110(2):251-60. [PubMed: 12150932] [MGI Ref ID J:78197]
Ripperger JA; Schibler U. 2006. Rhythmic CLOCK-BMAL1 binding to multiple E-box motifs drives circadian Dbp transcription and chromatin transitions. Nat Genet 38(3):369-74. [PubMed: 16474407] [MGI Ref ID J:106791]
Schmutz I; Ripperger JA; Baeriswyl-Aebischer S; Albrecht U. 2010. The mammalian clock component PERIOD2 coordinates circadian output by interaction with nuclear receptors. Genes Dev 24(4):345-57. [PubMed: 20159955] [MGI Ref ID J:156994]
Shearman LP; Sriram S; Weaver DR; Maywood ES; Chaves I; Zheng B; Kume K; Lee CC; van der Horst GT; Hastings MH; Reppert SM. 2000. Interacting molecular loops in the mammalian circadian clock [see comments] Science 288(5468):1013-9. [PubMed: 10807566] [MGI Ref ID J:62075]
So AY; Bernal TU; Pillsbury ML; Yamamoto KR; Feldman BJ. 2009. Glucocorticoid regulation of the circadian clock modulates glucose homeostasis. Proc Natl Acad Sci U S A 106(41):17582-7. [PubMed: 19805059] [MGI Ref ID J:153700]
Spanagel R; Pendyala G; Abarca C; Zghoul T; Sanchis-Segura C; Magnone MC; Lascorz J; Depner M; Holzberg D; Soyka M; Schreiber S; Matsuda F; Lathrop M; Schumann G; Albrecht U. 2005. The clock gene Per2 influences the glutamatergic system and modulates alcohol consumption. Nat Med 11(1):35-42. [PubMed: 15608650] [MGI Ref ID J:95457]
Virag JA; Dries JL; Easton PR; Friesland AM; DeAntonio JH; Chintalgattu V; Cozzi E; Lehmann BD; Ding JM; Lust RM. 2010. Attenuation of myocardial injury in mice with functional deletion of the circadian rhythm gene mPer2. Am J Physiol Heart Circ Physiol 298(3):H1088-95. [PubMed: 20061537] [MGI Ref ID J:158425]
Viswambharan H; Carvas JM; Antic V; Marecic A; Jud C; Zaugg CE; Ming XF; Montani JP; Albrecht U; Yang Z. 2007. Mutation of the circadian clock gene Per2 alters vascular endothelial function. Circulation 115(16):2188-95. [PubMed: 17404161] [MGI Ref ID J:135908]
Yang S; Liu A; Weidenhammer A; Cooksey RC; McClain D; Kim MK; Aguilera G; Abel ED; Chung JH. 2009. The role of mPer2 clock gene in glucocorticoid and feeding rhythms. Endocrinology 150(5):2153-60. [PubMed: 19179447] [MGI Ref ID J:158068]
Yelamanchili SV; Pendyala G; Brunk I; Darna M; Albrecht U; Ahnert-Hilger G. 2006. Differential sorting of the vesicular glutamate transporter 1 into a defined vesicular pool is regulated by light signaling involving the clock gene Period2. J Biol Chem 281(23):15671-9. [PubMed: 16595674] [MGI Ref ID J:113744]
Zhang B; Kracker S; Yasuda T; Casola S; Vanneman M; Homig-Holzel C; Wang Z; Derudder E; Li S; Chakraborty T; Cotter SE; Koyama S; Currie T; Freeman GJ; Kutok JL; Rodig SJ; Dranoff G; Rajewsky K. 2012. Immune Surveillance and Therapy of Lymphomas Driven by Epstein-Barr Virus Protein LMP1 in a Mouse Model. Cell 148(4):739-51. [PubMed: 22341446] [MGI Ref ID J:181546]
Zhang J; Kaasik K; Blackburn MR; Lee CC. 2006. Constant darkness is a circadian metabolic signal in mammals. Nature 439(7074):340-3. [PubMed: 16421573] [MGI Ref ID J:104616]
Zheng B; Albrecht U; Kaasik K; Sage M; Lu W; Vaishnav S; Li Q; Sun ZS; Eichele G; Bradley A; Lee CC. 2001. Nonredundant roles of the mPer1 and mPer2 genes in the mammalian circadian clock. Cell 105(5):683-94. [PubMed: 11389837] [MGI Ref ID J:69769]
Bradley A; Rachel RA. 2007. The albino B6 line, C57BL/6-Tyr<c-Brd> MGI Direct Data Submission :. [MGI Ref ID J:115975]
Jukkola PI; Rogers JT; Kaspar BK; Weeber EJ; Nishijima I. 2011. Secretin deficiency causes impairment in survival of neural progenitor cells in mice. Hum Mol Genet 20(5):1000-7. [PubMed: 21159798] [MGI Ref ID J:169029]
Lei L; Sonabend AM; Guarnieri P; Soderquist C; Ludwig T; Rosenfeld S; Bruce JN; Canoll P. 2011. Glioblastoma Models Reveal the Connection between Adult Glial Progenitors and the Proneural Phenotype. PLoS One 6(5):e20041. [PubMed: 21625383] [MGI Ref ID J:172585]
Liu P; Zhang H; McLellan A; Vogel H; Bradley A. 1998. Embryonic lethality and tumorigenesis caused by segmental aneuploidy on mouse chromosome 11. Genetics 150(3):1155-68. [PubMed: 9799267] [MGI Ref ID J:50799]
Martinez-Corral I; Olmeda D; Dieguez-Hurtado R; Tammela T; Alitalo K; Ortega S. 2012. In vivo imaging of lymphatic vessels in development, wound healing, inflammation, and tumor metastasis. Proc Natl Acad Sci U S A 109(16):6223-8. [PubMed: 22474390] [MGI Ref ID J:183610]
Mojumder DK; Wensel TG. 2010. Topical mydriatics affect light-evoked retinal responses in anesthetized mice. Invest Ophthalmol Vis Sci 51(1):567-76. [PubMed: 19661232] [MGI Ref ID J:160431]
Molina J; Carmona-Mora P; Chrast J; Krall PM; Canales CP; Lupski JR; Reymond A; Walz K. 2008. Abnormal social behaviors and altered gene expression rates in a mouse model for Potocki-Lupski syndrome. Hum Mol Genet 17(16):2486-95. [PubMed: 18469339] [MGI Ref ID J:138598]
Paylor R; Glaser B; Mupo A; Ataliotis P; Spencer C; Sobotka A; Sparks C; Choi CH; Oghalai J; Curran S; Murphy KC; Monks S; Williams N; O'Donovan MC; Owen MJ; Scambler PJ; Lindsay E. 2006. Tbx1 haploinsufficiency is linked to behavioral disorders in mice and humans: implications for 22q11 deletion syndrome. Proc Natl Acad Sci U S A 103(20):7729-34. [PubMed: 16684884] [MGI Ref ID J:110101]
Prosser HM; Bradley A; Chesham JE; Ebling FJ; Hastings MH; Maywood ES. 2007. Prokineticin receptor 2 (Prokr2) is essential for the regulation of circadian behavior by the suprachiasmatic nuclei. Proc Natl Acad Sci U S A 104(2):648-53. [PubMed: 17202262] [MGI Ref ID J:119071]
Walz K; Paylor R; Yan J; Bi W; Lupski JR. 2006. Rai1 duplication causes physical and behavioral phenotypes in a mouse model of dup(17)(p11.2p11.2). J Clin Invest 116(11):3035-41. [PubMed: 17024248] [MGI Ref ID J:114996]
Whitlock NA; Harrison B; Mixon T; Yu XQ; Wilson A; Gerhardt B; Eberhart DE; Abuin A; Rice DS. 2009. Decreased intraocular pressure in mice following either pharmacological or genetic inhibition of ROCK. J Ocul Pharmacol Ther 25(3):187-94. [PubMed: 19456252] [MGI Ref ID J:186058]
Yu YE; Wen L; Silva J; Li Z; Head K; Sossey-Alaoui K; Pao A; Mei L; Cowell JK. 2010. Lgi1 null mutant mice exhibit myoclonic seizures and CA1 neuronal hyperexcitability. Hum Mol Genet 19(9):1702-11. [PubMed: 20130004] [MGI Ref ID J:158715]
Zheng B; Mills AA; Bradley A. 1999. A system for rapid generation of coat color-tagged knockouts and defined chromosomal rearrangements in mice. Nucleic Acids Res 27(11):2354-60. [PubMed: 10325425] [MGI Ref ID J:115976]
Health & husbandry
Health & Colony Maintenance Information
Animal Health Reports
Room Number MGL375
Colony Maintenance
Breeding & Husbandry This strain originated on a B6;129S background and mice were backcrossed to C57BL/6-Tyrc-Brd mice (also called C57BL/6Brd-Tyrc-Brd) for several generations before being made homozygous for both the Per2tm1Brd targeted mutation on chromosome 1 and the the recessive Tyrc-Brd mutation on chromosome 7. When maintaining a live colony, homozygous mice may be bred together. By 9-12 months of age, homozygous females exhibit low reproductive success and produce small litters when compared to wildtype. These mice also carry the recessive Tyrc-Brd mutation that, when homozygous, results in albino coat color. Mating System Homozygote x Homozygote (Female x Male) 01-MAR-06
Pricing and Purchasing
Pricing, Supply Level & Notes, Controls
| Pricing for USA, Canada and Mexico shipping destinations |
|
Live Mice
Price per mouse (US dollars $) Gender Genotypes Provided Individual Mouse $177.00 Female or Male Homozygous for Per2tm1Brd
Price per Pair (US dollars $) Pair Genotype $354.00 Homozygous for Per2tm1Brd x Homozygous for Per2tm1Brd Standard Supply
Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
| Pricing for International shipping destinations |
|
Live Mice
Price per mouse (US dollars $) Gender Genotypes Provided Individual Mouse $230.10 Female or Male Homozygous for Per2tm1Brd
Price per Pair (US dollars $) Pair Genotype $460.20 Homozygous for Per2tm1Brd x Homozygous for Per2tm1Brd Standard Supply
Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
|
|
|
Standard Supply
Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
General Supply Notes
- Genomic DNA is available for this strain from the Mouse DNA Resource.
Control Information
| Control | ||
|---|---|---|
| 000058 B6(Cg)-Tyrc-2J/J | ||
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
| Control Pricing Information for Genetically Engineered Mutant Strains. | ||
Payment Terms and Conditions
Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.
See Terms of Use tab for General Terms and Conditions
The Jackson Laboratory's Genotype Promise
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.Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form
Terms of Use
Terms of Use
General Terms and Conditions
For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.
Contact information
General inquiries regarding Terms of UseContracts Administration
| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
JAX® Mice, Products & Services Conditions of Use
"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.No Warranty
MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.
In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.
No Liability
In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.
MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.
The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.
Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.