Strain Name:

C57BL/6J-Clockm1Jt/J

Stock Number:

002923

Order this mouse

Availability:

Cryopreserved - Ready for recovery

Other products are available, see Purchasing Information for Cryopreserved Embryos

Use Restrictions Apply, see Terms of Use

Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Chemically Induced Mutation; Coisogenic; Mutant Strain;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Specieslaboratory mouse
Background Strain C57BL/6J
 
Donating InvestigatorDr. Joseph S. Takahashi,   Univ Texas Southwestern Medical Ctr

Description
Mice heterozygous for this Clockdelta19 mutation (also called Clockmut or Clockm1Jt) show a lengthening of their circadian period by about 1 hour. Homozygous mice show a lengthening of 4 hours followed by a loss of circadian rhythm. Homozygous mice are viable. Male homozygotes are fertile, but female homozygotes appear to have reduced fertility.

Development
ENU-mutagenesis of male C57BL/6J mice created an A to T transversion at the third base position of the 5' splice donor site of intron 19. Exon 19 is missing from Clock mRNA, causing a 51 amino acid deletion within the glutamine-rich region of the protein's C terminus (amino acids 514-564). Mice with this Clockdelta19 mutation (also called Clockmut or Clockm1Jt) maintained on the C57BL/6J genetic background prior to sending to The Jackson Laboratory Repository.

Control Information

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

Related Strains

Strains carrying   Clockm1Jt allele
016175   C.B6-Clockm1Jt/J
View Strains carrying   Clockm1Jt     (1 strain)

Strains carrying other alleles of Clock
010925   B6.129S4-Clocktm1.1Rep/J
010490   B6.129S4-Clocktm1Rep/J
016167   B6.Cg-ClockGt(P007F12)Wrst/JtJ
016182   B6.Cg-Clocktm1Jt/J
008277   B6.Cg-Tg(tetO-Clockm1Jt)CL57Jt/J
008278   C57BL/6J-Tg(tetO-Clock)1Jt/J
View Strains carrying other alleles of Clock     (6 strains)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Clockm1Jt/Clock+

        C57BL/6-Clockm1Jt
  • behavior/neurological phenotype
  • abnormal behavior
    • in a forced-swim test, female mice exhibit less immobility compared with wild-type mice but as much as in Clockm1Jt homozygotes   (MGI Ref ID J:101849)
    • however, anxiety and depressive-like behavior are not increased   (MGI Ref ID J:101849)
    • abnormal circadian phase
      • in constant darkness, mice exhibit a 1 hour increase in free-running rhythm of locomotor activity compared with wild-type mice   (MGI Ref ID J:98343)
    • abnormal sleep pattern
      • mice spend 9% less time asleep during the entire 24 hour light dark cycle compared with wild-type mice   (MGI Ref ID J:65198)
      • during the 12 hour dark phase, mice spend less time in non-REM sleep than wild-type mice   (MGI Ref ID J:65198)
      • during the 12 hour dark phase, REM sleep is shorter than in wild-type mice   (MGI Ref ID J:65198)
    • increased exploration in new environment
      • during constant darkness in an open field, mice spend more time exploring the center than wild-type mice but as much as in Clockm1Jt homozygotes   (MGI Ref ID J:101849)
    • increased vertical activity
      • in female mice in an open field test   (MGI Ref ID J:101849)
    • prolonged circadian period
      • circadian period gradually lengthens over the first 39 days of constant darkness, with an average of 24.4 hours compared to 23.2 hours in wild-type   (MGI Ref ID J:18005)
      • increased 0.6 hr upon exposure to constant darkness   (MGI Ref ID J:198519)
      • mice on a C57BL/6J isogenic background exhibit a longer activity period under constant darkness than mice on a (BALB/cJ x C57BL/6J)F1 or BALB/cJ congenic background   (MGI Ref ID J:198519)

Clockm1Jt/Clock+

        involves: C57BL/6
  • homeostasis/metabolism phenotype
  • abnormal circulating protein level
    • mice exhibit decreased plasminogen activator inhibitor-1 (PAI-1) levels compared with wild-type mice   (MGI Ref ID J:155089)
    • at zeitgeber time (ZT) 14, mice fail to exhibit a decreased in total plasma tissue plasminogen activator (tPA) levels compared with wild-type mice   (MGI Ref ID J:155089)
  • abnormal response to injury
    • diurnal variations in time to thrombotic vascular occlusion (TTVO) subsequent to photochemical injury observed in similarly treated wild-type mice   (MGI Ref ID J:155089)
    • TTVO subsequent to photochemical injury is increased at zeitgeber time (ZT) 14 compared with similarly treated wild-type mice   (MGI Ref ID J:155089)
  • behavior/neurological phenotype
  • abnormal circadian rhythm
    • diurnal variations in thrombotic vascular occlusion subsequent to photochemical injury observed in similarly treated wild-type mice   (MGI Ref ID J:155089)

Clockm1Jt/Clock+

        B6(C)-Clockm1Jt
  • behavior/neurological phenotype
  • prolonged circadian period
    • under constant darkness, mice on a C57BL/6 congenic background exhibit prolonged activity periods compared with mice on a congenic BALB/cJ background   (MGI Ref ID J:198519)

Clockm1Jt/Clockm1Jt

        C57BL/6-Clockm1Jt
  • behavior/neurological phenotype
  • abnormal behavior
    • in a forced-swim test, female mice exhibit less immobility compared with wild-type mice   (MGI Ref ID J:101849)
    • in constant darkness, female mice exhibit reduced immobility in a forced-swim test compared with similarly treated wild-type mice   (MGI Ref ID J:101849)
    • however, anxiety and depressive-like behavior are not increased   (MGI Ref ID J:101849)
    • abnormal circadian rhythm
      • under dark dark conditions, mice spend more time awake than similarly treated wild-type mice   (MGI Ref ID J:65198)
      • delta energy accumulates over 28 hours unlike 24 in wild-type mice   (MGI Ref ID J:65198)
      • abnormal circadian phase
        • in constant darkness, mice exhibit a 3 to 4 hour increase in free-running rhythm of locomotor activity compared with wild-type mice   (MGI Ref ID J:98343)
        • after a few weeks in constant darkness, mice exhibit a break-down in circadian rhymicity unlike similarly treated wild-type mice   (MGI Ref ID J:98343)
        • mice exhibit a change in the temporal pattern of total activity during the dark phase with attenuation of the two peaks of activity normally observed in wild-type mice   (MGI Ref ID J:98343)
        • as early as 3 weeks of age, diurnal rhythm of food intake is severely altered with only a 53% increase in food intake during the dark phase compared with 75% in wild-type mice   (MGI Ref ID J:98343)
      • abnormal circadian regulation of heart rate
        • diurnal variation in heart rate is disrupted during the dark phase   (MGI Ref ID J:125921)
      • abnormal circadian regulation of systemic arterial blood pressure
        • diurnal variation in mean arterial pressure is disrupted during the light phase   (MGI Ref ID J:125921)
      • arrhythmic circadian persistence
        • the long circadian period is followed by a complete loss of circadian rhythmicity after about 2 weeks in constant darkness, although a residual ultradian periodicity of 6-9 hours remains   (MGI Ref ID J:18005)
      • prolonged circadian period
        • mutants exhibit extremely long circadian periods of 26 to 29 hours on initial transfer to constant darkness   (MGI Ref ID J:18005)
    • abnormal eating behavior
      • when fed a high fat diet during the light and dark phase   (MGI Ref ID J:98343)
      • abnormal food intake
        • food intake is increased during the light period and decreased during the dark phase compared with wild-type mice   (MGI Ref ID J:98343)
    • abnormal locomotor activation
      • activity levels are increased during the light period and decreased during the dark phase compared with wild-type mice   (MGI Ref ID J:98343)
      • hyperactivity
        • in female mice   (MGI Ref ID J:101849)
        • during the light phase   (MGI Ref ID J:98343)
      • increased vertical activity
        • in female mice in an open field test   (MGI Ref ID J:101849)
    • abnormal sleep pattern
      • mice spend 18% less time asleep during the entire 24 hour light dark cycle compared with wild-type mice   (MGI Ref ID J:65198)
      • during the 12 hour light and 12 hour dark phases, mice spend less time in non-REM sleep than wild-type mice   (MGI Ref ID J:65198)
      • during the 12 hour dark phase, REM sleep is longer than in wild-type mice   (MGI Ref ID J:65198)
      • during the 12 hour light phase, sleep episodes are shorter than in wild-type mice   (MGI Ref ID J:65198)
      • whether sleep deprived or not, total NREM delta energy is decreased compared to in wild-type mice   (MGI Ref ID J:65198)
      • under dark dark conditions, mice spend more time awake and less time in NREM sleep than wild-type mice   (MGI Ref ID J:65198)
      • delta energy accumulates over 28 hours unlike 24 in wild-type mice   (MGI Ref ID J:65198)
      • following sleep deprivation, mice exhibit less sleep and spend less time in REM sleep during the 12 hour dark phase compared with similarly treated wild-type mice   (MGI Ref ID J:65198)
    • increased exploration in new environment
      • during constant darkness in an open field, mice spend more time exploring the center than wild-type mice   (MGI Ref ID J:101849)
      • in an elevated plus maze, female mice exhibit increased number of arm entries compared with wild-type mice   (MGI Ref ID J:101849)
  • homeostasis/metabolism phenotype
  • abnormal basal metabolism
    • metabolic rate is increased during the light period and decreased during the dark phase compared with wild-type mice   (MGI Ref ID J:98343)
  • decreased circulating corticosterone level   (MGI Ref ID J:98343)
  • decreased energy expenditure
    • 10% overall   (MGI Ref ID J:98343)
    • increased susceptibility to diet-induced obesity
      • when fed a high fat diet, mice exhibit increased obesity with decreased gains in lean mass and increased gains in fat mass compared with similarly treated wild-type mice   (MGI Ref ID J:98343)
      • by 6 weeks, mice fed a high fat diet is increased compared to in similarly treated wild-type mice   (MGI Ref ID J:98343)
  • increased circulating cholesterol level
    • at 6 to 7 months when fed a regular diet   (MGI Ref ID J:98343)
  • increased circulating glucose level
    • at 6 to 7 months when fed a regular diet   (MGI Ref ID J:98343)
  • increased circulating leptin level
    • during the light phase when fed a regular and during the light and dark phase when fed a high fat diet   (MGI Ref ID J:98343)
  • increased circulating triglyceride level
    • at 6 to 7 months when fed a regular diet   (MGI Ref ID J:98343)
  • cardiovascular system phenotype
  • abnormal circadian regulation of heart rate
    • diurnal variation in heart rate is disrupted during the dark phase   (MGI Ref ID J:125921)
  • abnormal circadian regulation of systemic arterial blood pressure
    • diurnal variation in mean arterial pressure is disrupted during the light phase   (MGI Ref ID J:125921)
  • decreased heart rate
    • only during the active phase   (MGI Ref ID J:125921)
  • adipose tissue phenotype
  • increased fat cell size
    • when fed a high fat diet   (MGI Ref ID J:98343)
  • increased percent body fat
    • when fed a high fat diet, mice exhibit a 75% increase in fat mass compared with 25% in similarly treated wild-type mice   (MGI Ref ID J:98343)
  • growth/size/body phenotype
  • increased body weight
    • when fed a regular or high fat diet   (MGI Ref ID J:98343)
  • increased percent body fat
    • when fed a high fat diet, mice exhibit a 75% increase in fat mass compared with 25% in similarly treated wild-type mice   (MGI Ref ID J:98343)
  • increased susceptibility to diet-induced obesity
    • when fed a high fat diet, mice exhibit increased obesity with decreased gains in lean mass and increased gains in fat mass compared with similarly treated wild-type mice   (MGI Ref ID J:98343)
    • by 6 weeks, mice fed a high fat diet is increased compared to in similarly treated wild-type mice   (MGI Ref ID J:98343)
  • liver/biliary system phenotype
  • abnormal hepatocyte physiology
    • when mice are fed a high fat diet, hepatocytes exhibit lipid engorgement and glycogen accumulation compared with similarly treated wild-type mice   (MGI Ref ID J:98343)
  • hepatic steatosis
    • when fed a high fat diet   (MGI Ref ID J:98343)

Clockm1Jt/Clockm1Jt

        involves: C57BL/6
  • homeostasis/metabolism phenotype
  • abnormal glucose homeostasis
    • diurnal variation in glucose levels is disrupted   (MGI Ref ID J:131694)
    • fail to display a significant time dependent variation in their response to glucose or insulin   (MGI Ref ID J:131694)
    • do not develop frank diabetes when fed a high fat diet   (MGI Ref ID J:131694)
    • abnormal gluconeogenesis
    • increased insulin sensitivity
      • profound hypoglycemic response regardless of the time of day   (MGI Ref ID J:131694)
  • abnormal lipid homeostasis
    • diurnal variation in triglyceride levels is disrupted   (MGI Ref ID J:131694)
  • abnormal luteinizing hormone level
    • mice fail to exhibit an increase in luteinizing hormone level on the day of proestrus unlike wild-type mice   (MGI Ref ID J:92343)
    • estradiol benzoate-injected mice fail to exhibit a surge in luteinizing hormone unlike similarly treated wild-type mice   (MGI Ref ID J:92343)
    • however, elevation of luteinizing hormone in response to gonadotropin-releasing hormone treatment is normal   (MGI Ref ID J:92343)
    • decreased circulating luteinizing hormone level
      • estradiol benzoate-injected mice fail to exhibit a surge in luteinizing hormone unlike similarly treated wild-type mice   (MGI Ref ID J:92343)
      • however, elevation of luteinizing hormone in response to gonadotropin-releasing hormone treatment is normal   (MGI Ref ID J:92343)
  • decreased circulating estradiol level
    • during diestrus and post-coitus days 11 and 17   (MGI Ref ID J:92343)
  • decreased circulating progesterone level
    • during proestrus   (MGI Ref ID J:92343)
  • decreased physiological sensitivity to xenobiotic
    • estradiol benzoate-injected mice fail to exhibit a surge in luteinizing hormone unlike similarly treated wild-type mice   (MGI Ref ID J:92343)
    • however, elevation of luteinizing hormone in response to gonadotropin-releasing hormone treatment is normal   (MGI Ref ID J:92343)
  • increased circulating estradiol level
    • during proestrus   (MGI Ref ID J:92343)
  • increased circulating progesterone level
    • during proestrus   (MGI Ref ID J:92343)
  • behavior/neurological phenotype
  • abnormal circadian rhythm
    • when kept in darkness for intervals of 10 days mice exhibit reduced amplitude compared to similarly treated wild-type mice, especially after the second 10-day interval   (MGI Ref ID J:40363)
    • abnormal circadian phase
      • mice exhibit more activity throughout the light and dark cycle with more pronounced differences at the beginning of the dark cycle and the beginning of the light cycle compared with wild-type mice   (MGI Ref ID J:99868)
    • prolonged circadian period   (MGI Ref ID J:40363)
  • abnormal response to new environment
    • in a novel environment, locomotor activity increased compared to in wild-type mice   (MGI Ref ID J:99868)
  • enhanced behavioral response to cocaine
    • following chronic cocaine treatment, behavioral sensitization is increased compared with similarly treated wild-type mice   (MGI Ref ID J:99868)
    • mice exhibit a greater of place conditioning to a lower dose of cocaine compared with similarly treated wild-type mice   (MGI Ref ID J:99868)
  • hyperactivity
    • in a novel environment   (MGI Ref ID J:99868)
  • increased vertical activity
    • in a novel environment   (MGI Ref ID J:99868)
  • reproductive system phenotype
  • *normal* reproductive system phenotype
    • ovarian tissue morphology is normal   (MGI Ref ID J:92343)
    • abnormal pregnancy
      • mid-gestation mice exhibit increased post-coitus day 14 and full-term rate of fetal resorption and pregnancy failure at full-term compared with wild-type mice   (MGI Ref ID J:92343)
      • pseudopregnancy is shortened compared to in similarly treated wild-type mice   (MGI Ref ID J:92343)
      • abnormal parturition
        • 43% of females exhibit an extended but non-productive labor or fail to enter labor and fully reabsorb full-term fetuses unlike wild-type mice   (MGI Ref ID J:92343)
    • prolonged estrous cycle   (MGI Ref ID J:92343)
    • prolonged estrus   (MGI Ref ID J:92343)
    • short proestrus   (MGI Ref ID J:92343)
  • nervous system phenotype
  • abnormal single cell response
    • dopamine cell firing and bursting are enhanced compared with wild-type mice   (MGI Ref ID J:99868)

Clockm1Jt/Clockm1Jt

        involves: C57BL/6 * C57BL/6J
  • integument phenotype
  • abnormal hair cycle
    • mice exhibit a delay in the first synchronized anagen that persists through out the hair cycle that is not as severe as in Arntltm1Bra homozygotes   (MGI Ref ID J:151782)
    • abnormal hair cycle anagen phase
      • the first synchronized anagen is delayed compared to in wild-type mice that is not as severe as in Arntltm1Bra homozygotes   (MGI Ref ID J:151782)

Clockm1Jt/Clockm1Jt

        C57BL/6J-Clockm1Jt/J
  • digestive/alimentary phenotype
  • abnormal enterocyte physiology
    • lipid absorption and secretion by enterocytes is greater than in wild-type cells   (MGI Ref ID J:153782)
  • abnormal intestinal absorption
    • peptide absorption is lower than in wild-type mice while absorption of glucose and lipid is higher   (MGI Ref ID J:153782)
    • abnormal glucose absorption
      • glucose absorption is higher than in wild-type mice   (MGI Ref ID J:153782)
    • abnormal intestinal lipid absorption
      • lipid absorption by enterocytes is increased compared to in wild-type mice   (MGI Ref ID J:153782)
  • homeostasis/metabolism phenotype
  • abnormal intestinal lipid absorption
    • lipid absorption by enterocytes is increased compared to in wild-type mice   (MGI Ref ID J:153782)

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

Clockm1Jt/Clockm1Jt

        involves: BALB/cJ * C57BL/6
  • behavior/neurological phenotype
  • arrhythmic circadian persistence
    • the long circadian period is followed by a complete loss of circadian rhythmicity after about 2 weeks in constant darkness, although a residual ultradian periodicity of 6-9 hours remains   (MGI Ref ID J:18005)
    • however, a single 6 hour light pulse, given after the loss of rhythmicity in constant darkness, can restore the long periodicity temporarily   (MGI Ref ID J:18005)
  • prolonged circadian period
    • mutants exhibit extremely long circadian periods of 26 to 29 hours on initial transfer to constant darkness   (MGI Ref ID J:18005)
  • nervous system phenotype
  • *normal* nervous system phenotype
    • mutants do not exhibit any gross developmental or anatomical defects in the suprachiasmatic nucleus   (MGI Ref ID J:18005)

Clockm1Jt/Clockm1Jt

        involves: C57BL/6 * Jcl:ICR
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • mice exhibit normal passive avoidance   (MGI Ref ID J:116792)
    • abnormal circadian rhythm
      • the acrophases of body temperature, spontaneous activity, and wake are delayed by 2 to 3 hours compared with in wild-type mice   (MGI Ref ID J:103663)
      • the acrophase of REM sleep is delayed 4.4 hours compared to in wild-type mice   (MGI Ref ID J:103663)
      • the difference in the acrophase between non-REM and REM sleep is 3.5 hours unlike in wild-type mice   (MGI Ref ID J:103663)
      • peak electroencephalogram delta power of non-REM sleep appears at the onset of the light period unlike in wild-type mice   (MGI Ref ID J:103663)
      • however, entrainment is intact   (MGI Ref ID J:103663)
      • the acrophase of body temperature, spontaneous activity, and sleep are delayed 2 to 3 hours compared to in wild-type mice   (MGI Ref ID J:116792)
      • abnormal circadian temperature homeostasis
        • during the first half of the dark period and at the end of the light period   (MGI Ref ID J:103663)
    • abnormal sleep pattern
      • the acrophase of REM sleep is delayed 4.4 hours compared to in wild-type mice   (MGI Ref ID J:103663)
      • the difference in the acrophase between non-REM and REM sleep is 3.5 hours unlike in wild-type mice   (MGI Ref ID J:103663)
      • peak electroencephalogram delta power of non-REM sleep appears at the onset of the light period unlike in wild-type mice   (MGI Ref ID J:103663)
      • mice spend less time in non-REM sleep with an increase in waking compared with wild-type mice   (MGI Ref ID J:103663)
    • abnormal spatial learning
      • escape latency in Morris water maze is increased compared to in wild-type mice   (MGI Ref ID J:116792)
    • hyperactivity
      • in an open field test   (MGI Ref ID J:116792)
    • increased vertical activity
      • in an open field test   (MGI Ref ID J:116792)
  • homeostasis/metabolism phenotype
  • abnormal circadian temperature homeostasis
    • during the first half of the dark period and at the end of the light period   (MGI Ref ID J:103663)

Clockm1Jt/Clockm1Jt

        involves: C57BL/6 * C57BL/6J * Jcl:ICR
  • behavior/neurological phenotype
  • abnormal circadian rhythm
    • under light light conditions during lactation, mice exhibit delayed phase angle of locomotor activity onset during early developmental periods compared with similarly treated wild-type mice   (MGI Ref ID J:125037)
    • however, treatment with melatonin restores phase angle onset   (MGI Ref ID J:125037)
    • abnormal circadian phase
      • under light light conditions during lactation, 2 of 30 mice exhibit arrhythmicity of spontaneous activity unlike similarly treated wild-type mice   (MGI Ref ID J:125037)

Clockm1Jt/Clockm1Jt

        involves: BALB/c * C57BL/6 * C57BL/6J * Jcl:ICR
  • behavior/neurological phenotype
  • abnormal circadian rhythm
    • kaolin-induced writhing day-night fluctuations are abolished and writhing is decreased during the inactive phase compared to in similarly treated wild-type mice   (MGI Ref ID J:128504)
  • homeostasis/metabolism phenotype
  • decreased physiological sensitivity to xenobiotic
    • kaolin-induced writhing day-night fluctuations are abolished and writhing is decreased during the inactive phase compared to in similarly treated wild-type mice   (MGI Ref ID J:128504)
    • however, kaolin-induced bradykinin production and blood pressure suppression are normal   (MGI Ref ID J:128504)

Clockm1Jt/Clockm1Jt

        involves: BALB/cJ * C57BL/6 * C57BL/6J
  • nervous system phenotype
  • abnormal medium spiny neuron morphology
    • nucleus accumbens medium spiny neurons have longer and more complex dendrites and exhibit reduced GluR1 expression than those of wild-type mice   (MGI Ref ID J:166742)
    • lithium treatment reverses the changes in dendritic morphology   (MGI Ref ID J:166742)
  • abnormal nervous system electrophysiology
    • phase coupling between nucleus accumbens low-gamma oscillatory activity and delta activity is disrupted and prelimbic cortex low-gamma cross-frequency phase coupling tends to be decreased   (MGI Ref ID J:166742)
    • mutant mice fail to display the nucleus accumbens low-gamma cross-frequency phase coupling observed in wild-type mice during behaviorally immobile periods   (MGI Ref ID J:166742)
    • mutants exhibit neuronal entrainment deficits in nucleus accumbens   (MGI Ref ID J:166742)
    • lithium treatment ameliorates the nucleus accumbens phase-signaling dysfunction   (MGI Ref ID J:166742)
  • abnormal nucleus accumbens morphology
    • nucleus accumbens medium spiny neurons have longer and more complex dendrites and exhibit reduced GluR1 expression than those of wild-type mice   (MGI Ref ID J:166742)

The following phenotype relates to a compound genotype created using this strain.
Contact JAX® Services jaxservices@jax.org for customized breeding options.

Clockm1Jt/Clock+ Usf1soc/Usf1+

        (BALB/cJ x C57BL/6J)F1
  • behavior/neurological phenotype
  • prolonged circadian period
    • increased 0.3 hr upon exposure to constant darkness   (MGI Ref ID J:198519)
    • mice on a (BALB/cJ x C57BL/6J)F1 background exhibit a shorted extension of activity period upon exposure to constant darkness compared with mice on a C57BL/6J congenic background   (MGI Ref ID J:198519)

Clockm1Jt/Clock+ Usf1soc/Usf1soc

        C.B6-Clockm1Jt
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • mice on a BALB/cJ congenic background exhibit normal activity period under constant darkness unlike mice on a C57BL/6J isogenic background   (MGI Ref ID J:198519)
View Research Applications

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

Clockm1Jt related

Neurobiology Research
Behavioral and Learning Defects
Circadian Rhythms

Reproductive Biology Research
Fertility Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Clockm1Jt
Allele Name Clock
Allele Type Chemically induced (ENU)
Common Name(s) Ck; Clockdelta19; Clockmut;
Mutation Made ByDr. Joseph Takahashi,   Univ Texas Southwestern Medical Ctr
Strain of OriginC57BL/6J
Gene Symbol and Name Clock, circadian locomotor output cycles kaput
Chromosome 5
Gene Common Name(s) 5330400M04Rik; KAT13D; RIKEN cDNA 5330400M04 gene; bHLHe8; mKIAA0334;
General Note Phenotypic Similarity to Human Syndrome: Delayed Sleep Phase Syndrome (J:125037).

Phenotypic Similarity to Human Syndrome: Bipolar disorder (J:166742).

Molecular Note ENU mutagenesis caused an A to T transversion at the third base position of the 5' splice donor site of intron 19. RT-PCR using primers for exon 15 and exon 21 detected shorter transcripts and no wild-type transcript in hypothalamus of homozygous mutant mice. Sequence analysis revealed that these shorter transcripts are missing exon 19. The authors predict the protein will be missing a 51 amino acid region within the carboxy terminus. [MGI Ref ID J:40364]

Genotyping

Genotyping Information

Genotyping Protocols

Clockm1Jt, Pyrosequencing
Clocktm1Jt, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Vitaterna MH; King DP; Chang AM; Kornhauser JM; Lowrey PL; McDonald JD; Dove WF; Pinto LH; Turek FW; Takahashi JS. 1994. Mutagenesis and mapping of a mouse gene, Clock, essential for circadian behavior. Science 264(5159):719-25. [PubMed: 8171325]  [MGI Ref ID J:18005]

Additional References

Antoch MP; Song EJ; Chang AM; Vitaterna MH; Zhao Y; Wilsbacher LD; Sangoram AM; King DP; Pinto LH; Takahashi JS. 1997. Functional identification of the mouse circadian Clock gene by transgenic BAC rescue. Cell 89(4):655-67. [PubMed: 9160756]  [MGI Ref ID J:40363]

King DP; Zhao Y; Sangoram AM; Wilsbacher LD; Tanaka M; Antoch MP; Steeves TD; Vitaterna MH; Kornhauser JM; Lowrey PL; Turek FW; Takahashi JS. 1997. Positional cloning of the mouse circadian clock gene. Cell 89(4):641-53. [PubMed: 9160755]  [MGI Ref ID J:40364]

Udo R; Hamada T; Horikawa K; Iwahana E; Miyakawa K; Otsuka K; Shibata S. 2004. The role of Clock in the plasticity of circadian entrainment. Biochem Biophys Res Commun 318(4):893-8. [PubMed: 15147955]  [MGI Ref ID J:90131]

Clockm1Jt related

Andrews JL; Zhang X; McCarthy JJ; McDearmon EL; Hornberger TA; Russell B; Campbell KS; Arbogast S; Reid MB; Walker JR; Hogenesch JB; Takahashi JS; Esser KA. 2010. CLOCK and BMAL1 regulate MyoD and are necessary for maintenance of skeletal muscle phenotype and function. Proc Natl Acad Sci U S A 107(44):19090-5. [PubMed: 20956306]  [MGI Ref ID J:166235]

Anea CB; Zhang M; Stepp DW; Simkins GB; Reed G; Fulton DJ; Rudic RD. 2009. Vascular disease in mice with a dysfunctional circadian clock. Circulation 119(11):1510-7. [PubMed: 19273720]  [MGI Ref ID J:166003]

Antoch MP; Song EJ; Chang AM; Vitaterna MH; Zhao Y; Wilsbacher LD; Sangoram AM; King DP; Pinto LH; Takahashi JS. 1997. Functional identification of the mouse circadian Clock gene by transgenic BAC rescue. Cell 89(4):655-67. [PubMed: 9160756]  [MGI Ref ID J:40363]

Beaule C; Swanstrom A; Leone MJ; Herzog ED. 2009. Circadian modulation of gene expression, but not glutamate uptake, in mouse and rat cortical astrocytes. PLoS One 4(10):e7476. [PubMed: 19829696]  [MGI Ref ID J:154095]

Bertolucci C; Cavallari N; Colognesi I; Aguzzi J; Chen Z; Caruso P; Foa A; Tosini G; Bernardi F; Pinotti M. 2008. Evidence for an overlapping role of CLOCK and NPAS2 transcription factors in liver circadian oscillators. Mol Cell Biol 28(9):3070-5. [PubMed: 18316400]  [MGI Ref ID J:135812]

Challet E; Takahashi JS; Turek FW. 2000. Nonphotic phase-shifting in clock mutant mice. Brain Res 859(2):398-403. [PubMed: 10719095]  [MGI Ref ID J:61117]

Cordes S; Gallistel CR. 2008. Intact interval timing in circadian CLOCK mutants. Brain Res 1227:120-7. [PubMed: 18602902]  [MGI Ref ID J:139724]

Cretenet G; Le Clech M; Gachon F. 2010. Circadian clock-coordinated 12 Hr period rhythmic activation of the IRE1alpha pathway controls lipid metabolism in mouse liver. Cell Metab 11(1):47-57. [PubMed: 20074527]  [MGI Ref ID J:157002]

Curtis AM; Cheng Y; Kapoor S; Reilly D; Price TS; Fitzgerald GA. 2007. Circadian variation of blood pressure and the vascular response to asynchronous stress. Proc Natl Acad Sci U S A 104(9):3450-5. [PubMed: 17360665]  [MGI Ref ID J:125921]

Doi M; Ishida A; Miyake A; Sato M; Komatsu R; Yamazaki F; Kimura I; Tsuchiya S; Kori H; Seo K; Yamaguchi Y; Matsuo M; Fustin JM; Tanaka R; Santo Y; Yamada H; Takahashi Y; Araki M; Nakao K; Aizawa S; Kobayashi M; Obrietan K; Tsujimoto G; Okamura H. 2011. Circadian regulation of intracellular G-protein signalling mediates intercellular synchrony and rhythmicity in the suprachiasmatic nucleus. Nat Commun 2:327. [PubMed: 21610730]  [MGI Ref ID J:205653]

Doi R; Oishi K; Ishida N. 2010. CLOCK regulates circadian rhythms of hepatic glycogen synthesis through transcriptional activation of Gys2. J Biol Chem 285(29):22114-21. [PubMed: 20430893]  [MGI Ref ID J:165365]

Dolatshad H; Campbell EA; O'Hara L; Maywood ES; Hastings MH; Johnson MH. 2006. Developmental and reproductive performance in circadian mutant mice. Hum Reprod 21(1):68-79. [PubMed: 16210390]  [MGI Ref ID J:106391]

Dzirasa K; Coque L; Sidor MM; Kumar S; Dancy EA; Takahashi JS; McClung CA; Nicolelis MA. 2010. Lithium ameliorates nucleus accumbens phase-signaling dysfunction in a genetic mouse model of mania. J Neurosci 30(48):16314-23. [PubMed: 21123577]  [MGI Ref ID J:166742]

Easton A; Arbuzova J; Turek FW. 2003. The circadian Clock mutation increases exploratory activity and escape-seeking behavior. Genes Brain Behav 2(1):11-9. [PubMed: 12882315]  [MGI Ref ID J:101849]

Fortier EE; Rooney J; Dardente H; Hardy MP; Labrecque N; Cermakian N. 2011. Circadian variation of the response of T cells to antigen. J Immunol 187(12):6291-300. [PubMed: 22075697]  [MGI Ref ID J:180411]

Gu X; Xing L; Shi G; Liu Z; Wang X; Qu Z; Wu X; Dong Z; Gao X; Liu G; Yang L; Xu Y. 2012. The circadian mutation PER2(S662G) is linked to cell cycle progression and tumorigenesis. Cell Death Differ 19(3):397-405. [PubMed: 21818120]  [MGI Ref ID J:203085]

Hamdan AM; Koyanagi S; Wada E; Kusunose N; Murakami Y; Matsunaga N; Ohdo S. 2012. Intestinal expression of mouse Abcg2/breast cancer resistance protein (BCRP) gene is under control of circadian clock-activating transcription factor-4 pathway. J Biol Chem 287(21):17224-31. [PubMed: 22396548]  [MGI Ref ID J:185630]

Herzog ED; Grace MS; Harrer C; Williamson J; Shinohara K; Block GD. 2000. The role of clock in the developmental expression of neuropeptides in the suprachiasmatic nucleus J Comp Neurol 424(1):86-98. [PubMed: 10888741]  [MGI Ref ID J:63453]

Horikawa K; Minami Y; Iijima M; Akiyama M; Shibata S. 2005. Rapid damping of food-entrained circadian rhythm of clock gene expression in clock-defective peripheral tissues under fasting conditions. Neuroscience 134(1):335-43. [PubMed: 15961241]  [MGI Ref ID J:104434]

Hughes ME; Hong HK; Chong JL; Indacochea AA; Lee SS; Han M; Takahashi JS; Hogenesch JB. 2012. Brain-specific rescue of Clock reveals system-driven transcriptional rhythms in peripheral tissue. PLoS Genet 8(7):e1002835. [PubMed: 22844252]  [MGI Ref ID J:188150]

Kennaway DJ; Boden MJ; Voultsios A. 2004. Reproductive performance in female Clock Delta19 mutant mice. Reprod Fertil Dev 16(8):801-10. [PubMed: 15740704]  [MGI Ref ID J:154436]

Kennaway DJ; Owens JA; Voultsios A; Varcoe TJ. 2006. Functional central rhythmicity and light entrainment, but not liver and muscle rhythmicity, are Clock independent. Am J Physiol Regul Integr Comp Physiol 291(4):R1172-80. [PubMed: 16709646]  [MGI Ref ID J:112417]

Kennaway DJ; Voultsios A; Varcoe TJ; Moyer RW. 2003. Melatonin and activity rhythm responses to light pulses in mice with the Clock mutation. Am J Physiol Regul Integr Comp Physiol 284(5):R1231-40. [PubMed: 12521925]  [MGI Ref ID J:83391]

Kim J; Matsunaga N; Koyanagi S; Ohdo S. 2009. Clock gene mutation modulates the cellular sensitivity to genotoxic stress through altering the expression of N-methylpurine DNA glycosylase gene. Biochem Pharmacol 78(8):1075-82. [PubMed: 19540206]  [MGI Ref ID J:154338]

King DP; Vitaterna MH; Chang AM; Dove WF; Pinto LH; Turek FW ; Takahashi JS. 1997. The mouse Clock mutation behaves as an antimorph and maps within the W19H deletion, distal of Kit. Genetics 146(3):1049-60. [PubMed: 9215907]  [MGI Ref ID J:41383]

King DP; Zhao Y; Sangoram AM; Wilsbacher LD; Tanaka M; Antoch MP; Steeves TD; Vitaterna MH; Kornhauser JM; Lowrey PL; Turek FW; Takahashi JS. 1997. Positional cloning of the mouse circadian clock gene. Cell 89(4):641-53. [PubMed: 9160755]  [MGI Ref ID J:40364]

Koizumi H; Kurabayashi N; Watanabe Y; Sanada K. 2013. Increased anxiety in offspring reared by circadian Clock mutant mice. PLoS One 8(6):e66021. [PubMed: 23776596]  [MGI Ref ID J:203343]

Kolker DE; Vitaterna MH; Fruechte EM; Takahashi JS; Turek FW. 2004. Effects of age on circadian rhythms are similar in wild-type and heterozygous Clock mutant mice. Neurobiol Aging 25(4):517-23. [PubMed: 15013573]  [MGI Ref ID J:102074]

Kondratov RV; Shamanna RK; Kondratova AA; Gorbacheva VY; Antoch MP. 2006. Dual role of the CLOCK/BMAL1 circadian complex in transcriptional regulation. FASEB J 20(3):530-2. [PubMed: 16507766]  [MGI Ref ID J:129714]

Koyanagi S; Hamdan AM; Horiguchi M; Kusunose N; Okamoto A; Matsunaga N; Ohdo S. 2011. cAMP-response element (CRE)-mediated transcription by activating transcription factor-4 (ATF4) is essential for circadian expression of the Period2 gene. J Biol Chem 286(37):32416-23. [PubMed: 21768648]  [MGI Ref ID J:176743]

Kudo T; Kawashima M; Tamagawa T; Shibata S. 2008. Clock mutation facilitates accumulation of cholesterol in the liver of mice fed a cholesterol and/or cholic acid diet. Am J Physiol Endocrinol Metab 294(1):E120-30. [PubMed: 17971517]  [MGI Ref ID J:131221]

Lin KK; Kumar V; Geyfman M; Chudova D; Ihler AT; Smyth P; Paus R; Takahashi JS; Andersen B. 2009. Circadian clock genes contribute to the regulation of hair follicle cycling. PLoS Genet 5(7):e1000573. [PubMed: 19629164]  [MGI Ref ID J:151782]

Low-Zeddies SS; Takahashi JS. 2001. Chimera analysis of the Clock mutation in mice shows that complex cellular integration determines circadian behavior. Cell 105(1):25-42. [PubMed: 11301000]  [MGI Ref ID J:68852]

Malkesman O; Austin DR; Chen G; Manji HK. 2009. Reverse translational strategies for developing animal models of bipolar disorder. Dis Model Mech 2(5-6):238-45. [PubMed: 19407332]  [MGI Ref ID J:149734]

Marcheva B; Ramsey KM; Buhr ED; Kobayashi Y; Su H; Ko CH; Ivanova G; Omura C; Mo S; Vitaterna MH; Lopez JP; Philipson LH; Bradfield CA; Crosby SD; JeBailey L; Wang X; Takahashi JS; Bass J. 2010. Disruption of the clock components CLOCK and BMAL1 leads to hypoinsulinaemia and diabetes. Nature 466(7306):627-31. [PubMed: 20562852]  [MGI Ref ID J:162641]

Matsunaga N; Itcho K; Hamamura K; Ikeda E; Ikeyama H; Furuichi Y; Watanabe M; Koyanagi S; Ohdo S. 2014. 24-hour rhythm of aquaporin-3 function in the epidermis is regulated by molecular clocks. J Invest Dermatol 134(6):1636-44. [PubMed: 24418925]  [MGI Ref ID J:210850]

McClung CA; Sidiropoulou K; Vitaterna M; Takahashi JS; White FJ; Cooper DC; Nestler EJ. 2005. Regulation of dopaminergic transmission and cocaine reward by the Clock gene. Proc Natl Acad Sci U S A 102(26):9377-81. [PubMed: 15967985]  [MGI Ref ID J:99868]

Miller BH; McDearmon EL; Panda S; Hayes KR; Zhang J; Andrews JL; Antoch MP; Walker JR; Esser KA; Hogenesch JB; Takahashi JS. 2007. Circadian and CLOCK-controlled regulation of the mouse transcriptome and cell proliferation. Proc Natl Acad Sci U S A 104(9):3342-7. [PubMed: 17360649]  [MGI Ref ID J:125900]

Miller BH; Olson SL; Levine JE; Turek FW; Horton TH; Takahashi JS. 2006. Vasopressin regulation of the proestrous luteinizing hormone surge in wild-type and clock mutant mice. Biol Reprod 75(5):778-84. [PubMed: 16870944]  [MGI Ref ID J:114469]

Miller BH; Olson SL; Turek FW; Levine JE; Horton TH; Takahashi JS. 2004. Circadian clock mutation disrupts estrous cyclicity and maintenance of pregnancy. Curr Biol 14(15):1367-73. [PubMed: 15296754]  [MGI Ref ID J:92343]

Mohawk JA; Baer ML; Menaker M. 2009. The methamphetamine-sensitive circadian oscillator does not employ canonical clock genes. Proc Natl Acad Sci U S A 106(9):3519-24. [PubMed: 19204282]  [MGI Ref ID J:146448]

Mongrain V; Ruan X; Dardente H; Fortier EE; Cermakian N. 2008. Clock-dependent and independent transcriptional control of the two isoforms from the mouse Rorgammagene. Genes Cells 13(12):1197-210. [PubMed: 19076641]  [MGI Ref ID J:146572]

Nakahata Y; Sahar S; Astarita G; Kaluzova M; Sassone-Corsi P. 2009. Circadian control of the NAD+ salvage pathway by CLOCK-SIRT1. Science 324(5927):654-7. [PubMed: 19286518]  [MGI Ref ID J:147996]

Nakamura W; Honma S; Shirakawa T; Honma K. 2002. Clock mutation lengthens the circadian period without damping rhythms in individual SCN neurons. Nat Neurosci 5(5):399-400. [PubMed: 11953751]  [MGI Ref ID J:109488]

Nakamura W; Yamazaki S; Nakamura TJ; Shirakawa T; Block GD; Takumi T. 2008. In vivo monitoring of circadian timing in freely moving mice. Curr Biol 18(5):381-5. [PubMed: 18334203]  [MGI Ref ID J:135998]

Naylor E; Bergmann BM; Krauski K; Zee PC; Takahashi JS; Vitaterna MH; Turek FW. 2000. The circadian clock mutation alters sleep homeostasis in the mouse J Neurosci 20(21):8138-43. [PubMed: 11050136]  [MGI Ref ID J:65198]

Noshiro M; Usui E; Kawamoto T; Sato F; Nakashima A; Ueshima T; Honda K; Fujimoto K; Honma S; Honma K; Makishima M; Kato Y. 2009. Liver X receptors (LXRalpha and LXRbeta) are potent regulators for hepatic Dec1 expression. Genes Cells 14(1):29-40. [PubMed: 19032342]  [MGI Ref ID J:146580]

Ochi M; Sono S; Sei H; Oishi K; Kobayashi H; Morita Y; Ishida N. 2003. Sex difference in circadian period of body temperature in Clock mutant mice with Jcl/ICR background. Neurosci Lett 347(3):163-6. [PubMed: 12875911]  [MGI Ref ID J:108037]

Ohkura N; Oishi K; Fukushima N; Kasamatsu M; Atsumi GI; Ishida N; Horie S; Matsuda J. 2006. Circadian clock molecules CLOCK and CRYs modulate fibrinolytic activity by regulating the PAI-1 gene expression. J Thromb Haemost 4(11):2478-85. [PubMed: 16970803]  [MGI Ref ID J:135849]

Oike H; Nagai K; Fukushima T; Ishida N; Kobori M. 2011. Feeding cues and injected nutrients induce acute expression of multiple clock genes in the mouse liver. PLoS One 6(8):e23709. [PubMed: 21901130]  [MGI Ref ID J:176138]

Oishi K; Atsumi G; Sugiyama S; Kodomari I; Kasamatsu M; Machida K; Ishida N. 2006. Disrupted fat absorption attenuates obesity induced by a high-fat diet in Clock mutant mice. FEBS Lett 580(1):127-30. [PubMed: 16343493]  [MGI Ref ID J:136766]

Oishi K; Fukui H; Ishida N. 2000. Rhythmic expression of BMAL1 mRNA is altered in Clock mutant mice: differential regulation in the suprachiasmatic nucleus and peripheral tissues. Biochem Biophys Res Commun 268(1):164-71. [PubMed: 10652231]  [MGI Ref ID J:60291]

Oishi K; Koyanagi S; Ohkura N. 2013. The molecular clock regulates circadian transcription of tissue factor gene. Biochem Biophys Res Commun 431(2):332-5. [PubMed: 23291174]  [MGI Ref ID J:198078]

Oishi K; Miyazaki K; Ishida N. 2002. Functional CLOCK is not involved in the entrainment of peripheral clocks to the restricted feeding: entrainable expression of mPer2 and BMAL1 mRNAs in the heart of Clock mutant mice on Jcl:ICR background. Biochem Biophys Res Commun 298(2):198. [PubMed: 12387815]  [MGI Ref ID J:79723]

Oishi K; Miyazaki K; Kadota K; Kikuno R; Nagase T; Atsumi G; Ohkura N; Azama T; Mesaki M; Yukimasa S; Kobayashi H; Iitaka C; Umehara T; Horikoshi M; Kudo T; Shimizu Y; Yano M; Monden M; Machida K; Matsuda J; Horie S; Todo T; Ishida N. 2003. Genome-wide expression analysis of mouse liver reveals CLOCK-regulated circadian output genes. J Biol Chem 278(42):41519-27. [PubMed: 12865428]  [MGI Ref ID J:119414]

Oishi K; Ohkura N; Amagai N; Ishida N. 2005. Involvement of circadian clock gene Clock in diabetes-induced circadian augmentation of plasminogen activator inhibitor-1 (PAI-1) expression in the mouse heart. FEBS Lett 579(17):3555-9. [PubMed: 15950223]  [MGI Ref ID J:99783]

Oishi K; Ohkura N; Sei H; Matsuda J; Ishida N. 2007. CLOCK regulates the circadian rhythm of kaolin-induced writhing behavior in mice. Neuroreport 18(18):1925-8. [PubMed: 18007188]  [MGI Ref ID J:128504]

Oishi K; Ohkura N; Wakabayashi M; Shirai H; Sato K; Matsuda J; Atsumi G; Ishida N. 2006. CLOCK is involved in obesity-induced disordered fibrinolysis in ob/ob mice by regulating PAI-1 gene expression. J Thromb Haemost 4(8):1774-80. [PubMed: 16879220]  [MGI Ref ID J:135847]

Oishi K; Shirai H; Ishida N. 2005. CLOCK is involved in the circadian transactivation of peroxisome-proliferator-activated receptor alpha (PPARalpha) in mice. Biochem J 386(Pt 3):575-81. [PubMed: 15500444]  [MGI Ref ID J:117516]

Ozaki N; Noshiro M; Kawamoto T; Nakashima A; Honda K; Fukuzaki-Dohi U; Honma S; Fujimoto K; Tanimoto K; Tanne K; Kato Y. 2012. Regulation of basic helix-loop-helix transcription factors Dec1 and Dec2 by RORalpha and their roles in adipogenesis. Genes Cells 17(2):109-21. [PubMed: 22244086]  [MGI Ref ID J:203608]

Pan X; Hussain MM. 2009. Clock is important for food and circadian regulation of macronutrient absorption in mice. J Lipid Res 50:1800-1813. [PubMed: 19387090]  [MGI Ref ID J:153782]

Pan X; Zhang Y; Wang L; Hussain MM. 2010. Diurnal regulation of MTP and plasma triglyceride by CLOCK is mediated by SHP. Cell Metab 12(2):174-86. [PubMed: 20674862]  [MGI Ref ID J:163076]

Pekovic-Vaughan V; Gibbs J; Yoshitane H; Yang N; Pathiranage D; Guo B; Sagami A; Taguchi K; Bechtold D; Loudon A; Yamamoto M; Chan J; van der Horst GT; Fukada Y; Meng QJ. 2014. The circadian clock regulates rhythmic activation of the NRF2/glutathione-mediated antioxidant defense pathway to modulate pulmonary fibrosis. Genes Dev 28(6):548-60. [PubMed: 24637114]  [MGI Ref ID J:209595]

Pitts S; Perone E; Silver R. 2003. Food-entrained circadian rhythms are sustained in arrhythmic Clk/Clk mutant mice. Am J Physiol Regul Integr Comp Physiol 285(1):R57-67. [PubMed: 12649127]  [MGI Ref ID J:109337]

Ramsey KM; Yoshino J; Brace CS; Abrassart D; Kobayashi Y; Marcheva B; Hong HK; Chong JL; Buhr ED; Lee C; Takahashi JS; Imai S; Bass J. 2009. Circadian clock feedback cycle through NAMPT-mediated NAD+ biosynthesis. Science 324(5927):651-4. [PubMed: 19299583]  [MGI Ref ID J:147991]

Ripperger JA; Jud C; Albrecht U. 2011. The daily rhythm of mice. FEBS Lett 585(10):1384-92. [PubMed: 21354419]  [MGI Ref ID J:172029]

Roybal K; Theobold D; Graham A; Dinieri JA; Russo SJ; Krishnan V; Chakravarty S; Peevey J; Oehrlein N; Birnbaum S; Vitaterna MH; Orsulak P; Takahashi JS; Nestler EJ; Carlezon WA Jr; McClung CA. 2007. From the Cover: Mania-like behavior induced by disruption of CLOCK. Proc Natl Acad Sci U S A 104(15):6406-11. [PubMed: 17379666]  [MGI Ref ID J:120839]

Rudic RD; McNamara P; Curtis AM; Boston RC; Panda S; Hogenesch JB; Fitzgerald GA. 2004. BMAL1 and CLOCK, two essential components of the circadian clock, are involved in glucose homeostasis. PLoS Biol 2(11):e377. [PubMed: 15523558]  [MGI Ref ID J:131694]

Sahar S; Masubuchi S; Eckel-Mahan K; Vollmer S; Galla L; Ceglia N; Masri S; Barth TK; Grimaldi B; Oluyemi O; Astarita G; Hallows WC; Piomelli D; Imhof A; Baldi P; Denu JM; Sassone-Corsi P. 2014. Circadian control of fatty acid elongation by SIRT1 protein-mediated deacetylation of acetyl-coenzyme A synthetase 1. J Biol Chem 289(9):6091-7. [PubMed: 24425865]  [MGI Ref ID J:209499]

Sei H; Oishi K; Chikahisa S; Kitaoka K; Takeda E; Ishida N. 2008. Diurnal amplitudes of arterial pressure and heart rate are dampened in Clock mutant mice and adrenalectomized mice. Endocrinology 149(7):3576-80. [PubMed: 18403480]  [MGI Ref ID J:145372]

Sei H; Oishi K; Morita Y; Ishida N. 2001. Mouse model for morningness/eveningness. Neuroreport 12(7):1461-4. [PubMed: 11388430]  [MGI Ref ID J:103663]

Sei H; Oishi K; Sano A; Seno H; Ohmori T; Morita Y; Ishida N. 2006. Clock mutant mice with Jcl/ICR background shows an impaired learning ability in water maze, but not in passive avoidance, at the beginning of dark phase. Congenit Anom (Kyoto) 46(2):81-5. [PubMed: 16732766]  [MGI Ref ID J:116792]

Sei H; Sano A; Oishi K; Fujihara H; Kobayashi H; Ishida N; Morita Y. 2003. Increase of hippocampal acetylcholine release at the onset of dark phase is suppressed in a mutant mice model of evening-type individuals. Neuroscience 117(4):785-9. [PubMed: 12654331]  [MGI Ref ID J:125668]

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]

Shearman LP; Weaver DR. 1999. Photic induction of Period gene expression is reduced in Clock mutant mice. Neuroreport 10(3):613-8. [PubMed: 10208599]  [MGI Ref ID J:54424]

Shi G; Xing L; Liu Z; Qu Z; Wu X; Dong Z; Wang X; Gao X; Huang M; Yan J; Yang L; Liu Y; Ptacek LJ; Xu Y. 2013. Dual roles of FBXL3 in the mammalian circadian feedback loops are important for period determination and robustness of the clock. Proc Natl Acad Sci U S A 110(12):4750-5. [PubMed: 23471982]  [MGI Ref ID J:194250]

Shimomura K; Kumar V; Koike N; Kim TK; Chong J; Buhr ED; Whiteley AR; Low SS; Omura C; Fenner D; Owens JR; Richards M; Yoo SH; Hong HK; Vitaterna MH; Bass J; Pletcher MT; Wiltshire T; Hogenesch J; Lowrey PL; Takahashi JS. 2013. Usf1, a suppressor of the circadian Clock mutant, reveals the nature of the DNA-binding of the CLOCK:BMAL1 complex in mice. Elife 2:e00426. [PubMed: 23580255]  [MGI Ref ID J:198519]

Shostak A; Meyer-Kovac J; Oster H. 2013. Circadian regulation of lipid mobilization in white adipose tissues. Diabetes 62(7):2195-203. [PubMed: 23434933]  [MGI Ref ID J:208543]

Spencer S; Torres-Altoro MI; Falcon E; Arey R; Marvin M; Goldberg M; Bibb JA; McClung CA. 2012. A mutation in CLOCK leads to altered dopamine receptor function. J Neurochem 123(1):124-34. [PubMed: 22757753]  [MGI Ref ID J:190583]

Spengler ML; Kuropatwinski KK; Comas M; Gasparian AV; Fedtsova N; Gleiberman AS; Gitlin II; Artemicheva NM; Deluca KA; Gudkov AV; Antoch MP. 2012. Core circadian protein CLOCK is a positive regulator of NF-kappaB-mediated transcription. Proc Natl Acad Sci U S A 109(37):E2457-65. [PubMed: 22895791]  [MGI Ref ID J:189804]

Sujino M; Masumoto K; Yamaguchi S; van der Horst GT; Okamura H; Inouye SI. 2003. Suprachiasmatic nucleus grafts restore circadian behavioral rhythms of genetically arrhythmic mice. Curr Biol 13(8):664-8. [PubMed: 12699623]  [MGI Ref ID J:82988]

Summa KC; Voigt RM; Forsyth CB; Shaikh M; Cavanaugh K; Tang Y; Vitaterna MH; Song S; Turek FW; Keshavarzian A. 2013. Disruption of the Circadian Clock in Mice Increases Intestinal Permeability and Promotes Alcohol-Induced Hepatic Pathology and Inflammation. PLoS One 8(6):e67102. [PubMed: 23825629]  [MGI Ref ID J:204345]

Takeda N; Maemura K; Horie S; Oishi K; Imai Y; Harada T; Saito T; Shiga T; Amiya E; Manabe I; Ishida N; Nagai R. 2007. Thrombomodulin is a clock-controlled gene in vascular endothelial cells. J Biol Chem 282(45):32561-7. [PubMed: 17848551]  [MGI Ref ID J:126950]

Tokizawa K; Uchida Y; Nagashima K. 2009. Thermoregulation in the cold changes depending on the time of day and feeding condition: physiological and anatomical analyses of involved circadian mechanisms. Neuroscience 164(3):1377-86. [PubMed: 19703527]  [MGI Ref ID J:155139]

Turek FW; Joshu C; Kohsaka A; Lin E; Ivanova G; McDearmon E; Laposky A; Losee-Olson S; Easton A; Jensen DR; Eckel RH; Takahashi JS; Bass J. 2005. Obesity and metabolic syndrome in circadian Clock mutant mice. Science 308(5724):1043-5. [PubMed: 15845877]  [MGI Ref ID J:98343]

Udo R; Hamada T; Horikawa K; Iwahana E; Miyakawa K; Otsuka K; Shibata S. 2004. The role of Clock in the plasticity of circadian entrainment. Biochem Biophys Res Commun 318(4):893-8. [PubMed: 15147955]  [MGI Ref ID J:90131]

Vitaterna MH; Ko CH; Chang AM; Buhr ED; Fruechte EM; Schook A; Antoch MP; Turek FW; Takahashi JS. 2006. The mouse Clock mutation reduces circadian pacemaker amplitude and enhances efficacy of resetting stimuli and phase-response curve amplitude. Proc Natl Acad Sci U S A 103(24):9327-32. [PubMed: 16754844]  [MGI Ref ID J:111042]

Wakatsuki Y; Kudo T; Shibata S. 2007. Constant light housing during nursing causes human DSPS (delayed sleep phase syndrome) behaviour in Clock-mutant mice. Eur J Neurosci 25(8):2413-24. [PubMed: 17445238]  [MGI Ref ID J:125037]

Westgate EJ; Cheng Y; Reilly DF; Price TS; Walisser JA; Bradfield CA; FitzGerald GA. 2008. Genetic components of the circadian clock regulate thrombogenesis in vivo. Circulation 117(16):2087-95. [PubMed: 18413500]  [MGI Ref ID J:155089]

Wilsbacher LD; Sangoram AM; Antoch MP; Takahashi JS. 2000. The mouse clock locus: sequence and comparative analysis of 204 Kb from mouse chromosome 5 Genome Res 10(12):1928-40. [PubMed: 11116088]  [MGI Ref ID J:66232]

Yu X; Rollins D; Ruhn KA; Stubblefield JJ; Green CB; Kashiwada M; Rothman PB; Takahashi JS; Hooper LV. 2013. TH17 cell differentiation is regulated by the circadian clock. Science 342(6159):727-30. [PubMed: 24202171]  [MGI Ref ID J:202881]

van Enkhuizen J; Minassian A; Young JW. 2013. Further evidence for ClockDelta19 mice as a model for bipolar disorder mania using cross-species tests of exploration and sensorimotor gating. Behav Brain Res 249:44-54. [PubMed: 23623885]  [MGI Ref ID J:198493]

Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Colony Maintenance

Breeding & HusbandryThis strain is maintained by backcrossing heterozygous males to C57BL/6J females. Homozygous females don't breed well. This strain is currently on a C57BL/6J background (4/23/97) Expected coat color from breeding:Black

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2525.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Frozen Products

Price (US dollars $)
Frozen Embryo $1650.00

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We willfulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3283.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Frozen Products

Price (US dollars $)
Frozen Embryo $2145.00

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We willfulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Control Information

  Control
   Wild-type from the colony
   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.

Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

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.


(6.6)