Overview

Also Known As:Clock

These mice carry an ENU-induced mutation characterized by a lengthening of their circadian period.

Donating Investigator

Dr. Joseph S. Takahashi, Univ Texas Southwestern Medical Ctr

Genetic overview

Genetic Background	Generation
000664 C57BL/6J

Clock^m1Jt

Allele Type	Gene Symbol	Gene Name
Chemically induced (ENU)	Clock	circadian locomotor output cycles kaput

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Research Applications

Neurobiology Research
Reproductive Biology Research

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

Mice heterozygous for this Clock^delta19 mutation (also called Clock^mut or Clock^m1Jt) 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 Clock^delta19 mutation (also called Clock^mut or Clock^m1Jt) maintained on the C57BL/6J genetic background prior to sending to The Jackson Laboratory Repository.

Control Suggestions

Wild-type from the colony
000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

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):719-25PubMed: 8171325 MGI: J:18005

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Genetics

Clock^m1Jt

Allele Symbol: Clock^m1Jt

Allele Name	Clock
Allele Type	Chemically induced (ENU)
Allele Synonym(s)	Ck; Clock^delta19; Clock^mut
Gene Symbol and Name	Clock, circadian locomotor output cycles kaput
Gene Synonym(s)
Strain of Origin	C57BL/6J
Chromosome	5
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.
Mutations Made By	Dr. Joseph Takahashi, Univ Texas Southwestern Medical Ctr

Disease/Phenotype

Disease Terms

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

Research Areas By Phenotype

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

Genotype: Clock^m1Jt related

Neurobiology Research
- Behavioral and Learning Defects
- Circadian Rhythms
Reproductive Biology Research
- Fertility Defects

Mammalian Phenotype Terms by Genotype

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

Genotype: Clock^m1Jt/Clock^m1Jt
involves: BALB/c * C57BL/6 * C57BL/6J * Jcl:ICR

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
- Normal - however, kaolin-induced bradykinin production and blood pressure suppression are normal

Genotype: Clock^m1Jt/Clock^m1Jt
involves: BALB/cJ * C57BL/6

behavior/neurological phenotype

arrhythmic circadian behavior 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
- however, a single 6 hour light pulse, given after the loss of rhythmicity in constant darkness, can restore the long periodicity temporarily

prolonged circadian behavior period
- mutants exhibit extremely long circadian periods of 26 to 29 hours on initial transfer to constant darkness

mammalian phenotype

nervous system phenotype
- Normal - mutants do not exhibit any gross developmental or anatomical defects in the suprachiasmatic nucleus

Genotype: Clock^m1Jt/Clock^m1Jt
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
- lithium treatment reverses the changes in dendritic morphology

abnormal nervous system electrophysiology
- lithium treatment ameliorates the nucleus accumbens phase-signaling dysfunction
- 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
- mutant mice fail to display the nucleus accumbens low-gamma cross-frequency phase coupling observed in wild-type mice during behaviorally immobile periods
- mutants exhibit neuronal entrainment deficits in nucleus accumbens

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

Genotype: Clock^m1Jt/Clock^m1Jt
involves: C57BL/6 * Jcl:ICR

homeostasis/metabolism phenotype

abnormal circadian temperature homeostasis
- the acrophase of body temperature is delayed by 2 to 3 hours compared with in wild-type mice
- during the first half of the dark period and at the end of the light period

mammalian phenotype

behavior/neurological phenotype
- Normal - mice exhibit normal passive avoidance

behavior/neurological phenotype

abnormal circadian sleep/wake cycle
- peak electroencephalogram delta power of non-REM sleep appears at the onset of the light period unlike in wild-type mice
- the acrophase of wake time is delayed by 2 to 3 hours compared with in wild-type mice
- the difference in the acrophase between non-REM and REM sleep is 3.5 hours unlike in wild-type mice
- the acrophase of REM sleep is delayed 4.4 hours compared to in wild-type mice

abnormal sleep pattern
- the acrophase of REM sleep is delayed 4.4 hours compared to in wild-type mice
- mice spend less time in non-REM sleep with an increase in waking compared with wild-type mice
- peak electroencephalogram delta power of non-REM sleep appears at the onset of the light period unlike in wild-type mice
- the difference in the acrophase between non-REM and REM sleep is 3.5 hours unlike in wild-type mice

abnormal spatial learning
- escape latency in Morris water maze is increased compared to in wild-type mice

hyperactivity
- in an open field test

abnormal circadian behavior
- the acrophase of spontaneous activity is delayed by 2 to 3 hours compared with in wild-type mice
- Normal - however, entrainment is intact

increased vertical activity
- in an open field test

Genotype: Clock^m1Jt/Clock^m1Jt
involves: C57BL/6 * C57BL/6J * Jcl:ICR

behavior/neurological phenotype

abnormal circadian behavior
- 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
- Normal - however, treatment with melatonin restores phase angle onset

abnormal circadian behavior phase
- under light light conditions during lactation, 2 of 30 mice exhibit arrhythmicity of spontaneous activity unlike similarly treated wild-type mice

Genotype: Clock^m1Jt/Clock⁺ Usf1^soc/Usf1⁺
(BALB/cJ x C57BL/6J)F1

behavior/neurological phenotype

prolonged circadian behavior period
- Background Sensitivity - 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
- increased 0.3 hr upon exposure to constant darkness

Genotype: Clock^m1Jt/Clock⁺ Usf1^soc/Usf1^soc
C.B6-Clock

mammalian phenotype

behavior/neurological phenotype
- Normal - mice on a BALB/cJ congenic background exhibit normal activity period under constant darkness unlike mice on a C57BL/6J isogenic background

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

Genotype: Clock^m1Jt/Clock⁺
involves: C57BL/6

homeostasis/metabolism phenotype

abnormal circulating protein level
- at zeitgeber time (ZT) 14, mice fail to exhibit a decreased in total plasma tissue plasminogen activator (tPA) levels compared with wild-type mice
- mice exhibit decreased plasminogen activator inhibitor-1 (PAI-1) levels compared with wild-type mice

abnormal response to injury
- TTVO subsequent to photochemical injury is increased at zeitgeber time (ZT) 14 compared with similarly treated wild-type mice
- diurnal variations in time to thrombotic vascular occlusion (TTVO) subsequent to photochemical injury observed in similarly treated wild-type mice

Genotype: Clock^m1Jt/Clock^m1Jt
involves: C57BL/6

behavior/neurological phenotype

abnormal circadian behavior
- 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

hyperactivity
- in a novel environment

abnormal response to new environment
- in a novel environment, locomotor activity increased compared to in wild-type mice

increased vertical activity
- in a novel environment

enhanced behavioral response to cocaine
- following chronic cocaine treatment, behavioral sensitization is increased compared with similarly treated wild-type mice
- mice exhibit a greater of place conditioning to a lower dose of cocaine compared with similarly treated wild-type mice

abnormal circadian behavior 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

prolonged circadian behavior period

homeostasis/metabolism phenotype

decreased circulating estradiol level
- during diestrus and post-coitus days 11 and 17

decreased circulating luteinizing hormone level
- Normal - however, elevation of luteinizing hormone in response to gonadotropin-releasing hormone treatment is normal
- estradiol benzoate-injected mice fail to exhibit a surge in luteinizing hormone unlike similarly treated wild-type mice

abnormal luteinizing hormone level
- mice fail to exhibit an increase in luteinizing hormone level on the day of proestrus unlike wild-type mice
- estradiol benzoate-injected mice fail to exhibit a surge in luteinizing hormone unlike similarly treated wild-type mice
- Normal - however, elevation of luteinizing hormone in response to gonadotropin-releasing hormone treatment is normal

decreased physiological sensitivity to xenobiotic
- estradiol benzoate-injected mice fail to exhibit a surge in luteinizing hormone unlike similarly treated wild-type mice
- Normal - however, elevation of luteinizing hormone in response to gonadotropin-releasing hormone treatment is normal

increased insulin sensitivity
- profound hypoglycemic response regardless of the time of day

abnormal glucose homeostasis
- do not develop frank diabetes when fed a high fat diet
- diurnal variation in glucose levels is disrupted
- fail to display a significant time dependent variation in their response to glucose or insulin

increased circulating progesterone level
- during proestrus

impaired gluconeogenesis

abnormal lipid homeostasis
- diurnal variation in triglyceride levels is disrupted

decreased circulating progesterone level
- during proestrus

increased circulating estradiol level
- during proestrus

mammalian phenotype

reproductive system phenotype
- Normal - ovarian tissue morphology is normal

nervous system phenotype

abnormal single cell response
- dopamine cell firing and bursting are enhanced compared with wild-type mice

reproductive system phenotype

abnormal pregnancy
- pseudopregnancy is shortened compared to in similarly treated wild-type mice
- 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

prolonged estrous cycle

short proestrus

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

prolonged estrus

Genotype: Clock^m1Jt/Clock^m1Jt
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 Arntl^tm1Bra homozygotes

abnormal hair cycle anagen phase
- the first synchronized anagen is delayed compared to in wild-type mice that is not as severe as in Arntl^tm1Bra homozygotes

Genotype: Clock^m1Jt/Clock⁺
C57BL/6-Clock

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 Clock^m1Jt homozygotes
- Normal - however, anxiety and depressive-like behavior are not increased

abnormal sleep pattern
- during the 12 hour dark phase, mice spend less time in non-REM sleep than wild-type mice
- mice spend 9% less time asleep during the entire 24 hour light dark cycle compared with wild-type mice
- during the 12 hour dark phase, REM sleep is shorter than in wild-type mice

increased vertical activity
- in female mice in an open field test

prolonged circadian behavior period
- Background Sensitivity - 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
- increased 0.6 hr upon exposure to constant darkness
- 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

abnormal circadian behavior phase
- in constant darkness, mice exhibit a 1 hour increase in free-running rhythm of locomotor activity compared with wild-type mice

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 Clock^m1Jt homozygotes

Genotype: Clock^m1Jt/Clock^m1Jt
C57BL/6J-Clock/J

digestive/alimentary phenotype

abnormal intestinal absorption
- peptide absorption is lower than in wild-type mice while absorption of glucose and lipid is higher

abnormal enterocyte physiology
- lipid absorption and secretion by enterocytes is greater than in wild-type cells

abnormal intestinal lipid absorption
- lipid absorption by enterocytes is increased compared to in wild-type mice

increased intestinal glucose absorption
- glucose absorption is higher than in wild-type mice

homeostasis/metabolism phenotype

abnormal intestinal lipid absorption
- lipid absorption by enterocytes is increased compared to in wild-type mice

Genotype: Clock^m1Jt/Clock^m1Jt
involves: C57BL/6J

cellular phenotype

increased pancreatic islet cell apoptosis
- trend toward increased islet apoptosis

homeostasis/metabolism phenotype

hyperglycemia
- Normal - however, fasting and fed glucose levels in 3 month old mice are normal
- mutants show elevated fasting glucose levels at both Zeitgeber time 2 and Zeitgeber time 14
- glucose levels are elevated across the entire light/dark cycle in 4 month old mutants without a rise in insulin levels during the beginning of the feeding period as is seen in wild-type mice

decreased insulin secretion
- islets from young mice show impaired glucose-stimulated insulin secretion
- islets from 8 month old mutants show an approximate 50% reduction in glucose-stimulated insulin secretion and fail to respond to KCl, indicating a defect in insulin exocytosis
- islets display diminished insulin secretory responses to the cyclase activators forskolin and exendin 4, and 8-bromo-cAMP

impaired glucose tolerance
- Normal - however, mice show normal insulin tolerance
- glucose tolerance tests show a 50% reduction in insulin release that corresponds with elevated glucose levels, particularly at the beginning of the dark period

increased insulin sensitivity
- 3 month old mice have enhanced insulin sensitivity

insulin resistance
- gradual onset of insulin resistance

endocrine/exocrine gland phenotype

abnormal pancreas physiology
- 23% decrease in proliferation of islets
- decrease in levels of expression and/or phase shifts of RNA oscillation of genes involved in insulin signaling, glucose sensing, and islet growth and development
- islets lack a circadian rhythm, even after forskolin stimulation

decreased insulin secretion
- islets display diminished insulin secretory responses to the cyclase activators forskolin and exendin 4, and 8-bromo-cAMP
- islets from young mice show impaired glucose-stimulated insulin secretion
- islets from 8 month old mutants show an approximate 50% reduction in glucose-stimulated insulin secretion and fail to respond to KCl, indicating a defect in insulin exocytosis

abnormal pancreatic islet morphology
- total islet area is reduced by around 20%
- trend toward decreased total pancreatic insulin content

small pancreatic islets

increased pancreatic islet cell apoptosis
- trend toward increased islet apoptosis

Genotype: Clock^m1Jt/Clock^m1Jt
C57BL/6-Clock

adipose tissue phenotype

increased percent body fat/body weight
- when fed a high fat diet, mice exhibit a 75% increase in fat mass compared with 25% in similarly treated wild-type mice

increased fat cell size
- when fed a high fat diet

cardiovascular system phenotype

abnormal circadian regulation of heart rate
- diurnal variation in heart rate is disrupted during the dark phase

abnormal circadian regulation of systemic arterial blood pressure
- diurnal variation in mean arterial pressure is disrupted during the light phase

decreased heart rate
- only during the active phase

growth/size/body region phenotype

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
- by 6 weeks, mice fed a high fat diet is increased compared to in similarly treated wild-type mice

increased body weight
- when fed a regular or high fat diet

homeostasis/metabolism phenotype

increased susceptibility to diet-induced obesity
- by 6 weeks, mice fed a high fat diet is increased compared to in similarly treated wild-type mice
- 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

decreased circulating corticosterone level

abnormal basal metabolism
- metabolic rate is increased during the light period and decreased during the dark phase compared with wild-type mice

decreased energy expenditure
- 10% overall

increased circulating cholesterol level
- at 6 to 7 months when fed a regular diet

increased circulating glucose level
- at 6 to 7 months when fed a regular diet

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

increased circulating triglyceride level
- at 6 to 7 months when fed a regular diet

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

hepatic steatosis
- when fed a high fat diet

behavior/neurological phenotype

abnormal circadian behavior
- under dark dark conditions, mice spend more time awake than similarly treated wild-type mice
- delta energy accumulates over 28 hours unlike 24 in wild-type mice

abnormal locomotor circadian rhythm
- activity levels are increased during the light period and decreased during the dark phase compared with wild-type mice

hyperactivity
- during the light phase
- in female mice

increased exploration in new environment
- during constant darkness in an open field, mice spend more time exploring the center than wild-type mice
- in an elevated plus maze, female mice exhibit increased number of arm entries compared with wild-type mice

abnormal circadian behavior phase
- after a few weeks in constant darkness, mice exhibit a break-down in circadian rhymicity unlike similarly treated wild-type mice
- 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
- 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
- in constant darkness, mice exhibit a 3 to 4 hour increase in free-running rhythm of locomotor activity compared with wild-type mice

abnormal sleep pattern
- during the 12 hour light and 12 hour dark phases, mice spend less time in non-REM sleep than wild-type mice
- delta energy accumulates over 28 hours unlike 24 in wild-type mice
- during the 12 hour light phase, sleep episodes are shorter than in wild-type mice
- whether sleep deprived or not, total NREM delta energy is decreased compared to in wild-type mice
- mice spend 18% less time asleep during the entire 24 hour light dark cycle compared with wild-type mice
- during the 12 hour dark phase, REM sleep is longer than in wild-type mice
- 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
- under dark dark conditions, mice spend more time awake and less time in NREM sleep than wild-type mice

abnormal behavior
- Normal - however, anxiety and depressive-like behavior are not increased
- in constant darkness, female mice exhibit reduced immobility in a forced-swim test compared with similarly treated wild-type mice
- in a forced-swim test, female mice exhibit less immobility compared with wild-type mice

abnormal circadian sleep/wake cycle
- delta energy accumulates over 28 hours unlike 24 in wild-type mice

prolonged circadian behavior period
- mutants exhibit extremely long circadian periods of 26 to 29 hours on initial transfer to constant darkness

abnormal circadian behavior 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

abnormal eating behavior
- when fed a high fat diet during the light and dark phase

abnormal food intake
- food intake is increased during the light period and decreased during the dark phase compared with wild-type mice

increased vertical activity
- in female mice in an open field test

Genotype: Clock^m1Jt/Clock⁺
B6(C)-Clock

behavior/neurological phenotype

prolonged circadian behavior period
- Background Sensitivity - under constant darkness, mice on a C57BL/6 congenic background exhibit prolonged activity periods compared with mice on a congenic BALB/cJ background

References

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):719-25PubMed: 8171325 MGI: 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):655-67PubMed: 9160756 MGI: 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):641-53PubMed: 9160755 MGI: 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):893-8PubMed: 15147955 MGI: J:90131

Additional - Clock^m1Jt related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Pyrosequencing:Clock
- Sanger sequencing:Clock-SEQ
- Standard PCR:Clock
- Genotyping resources and troubleshooting
Breeding Considerations

This 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
- Additional Breeding and Husbandry Support
Citation
When using the Clock mouse strain in a publication, please cite the originating article(s) and include JAX stock #002923 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

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

Pricing & Availability

Cryo Recovery

Domestic
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Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
> >	Heterozygous or Wildtype for Clock<m1Jt>

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Frozen Mouse Embryo	C57BL/6J-Clockm1Jt/J Frozen Embryos	$2595.00
Frozen Mouse Embryo	C57BL/6J-Clockm1Jt/J Frozen Embryos	$2595.00
Frozen Mouse Embryo	C57BL/6J-Clockm1Jt/J Frozen Embryos	$3373.50
Frozen Mouse Embryo	C57BL/6J-Clockm1Jt/J Frozen Embryos	$3373.50

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

Terms Of Use

General Terms and Conditions

Questions about Terms of Use

Additional Use Restrictions Apply

Use of MICE by companies or for-profit entities requires a license.

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:Clock

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Clockm1Jt

Allele Symbol: Clockm1Jt

Disease Terms

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

Research Areas By Phenotype

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

Genotype: Clockm1Jt related

Mammalian Phenotype Terms by Genotype

Genotype: Clockm1Jt/Clockm1Jtinvolves: BALB/c * C57BL/6 * C57BL/6J * Jcl:ICR

homeostasis/metabolism phenotype

Genotype: Clockm1Jt/Clockm1Jtinvolves: BALB/cJ * C57BL/6

behavior/neurological phenotype

mammalian phenotype

Genotype: Clockm1Jt/Clockm1Jtinvolves: BALB/cJ * C57BL/6 * C57BL/6J

nervous system phenotype

Genotype: Clockm1Jt/Clockm1Jtinvolves: C57BL/6 * Jcl:ICR

homeostasis/metabolism phenotype

mammalian phenotype

behavior/neurological phenotype

Genotype: Clockm1Jt/Clockm1Jtinvolves: C57BL/6 * C57BL/6J * Jcl:ICR

behavior/neurological phenotype

Genotype: Clockm1Jt/Clock+ Usf1soc/Usf1+(BALB/cJ x C57BL/6J)F1

behavior/neurological phenotype

Genotype: Clockm1Jt/Clock+ Usf1soc/Usf1socC.B6-Clock

mammalian phenotype

Genotype: Clockm1Jt/Clock+involves: C57BL/6

homeostasis/metabolism phenotype

Genotype: Clockm1Jt/Clockm1Jtinvolves: C57BL/6

behavior/neurological phenotype

homeostasis/metabolism phenotype

mammalian phenotype

nervous system phenotype

reproductive system phenotype

Genotype: Clockm1Jt/Clockm1Jtinvolves: C57BL/6 * C57BL/6J

integument phenotype

Genotype: Clockm1Jt/Clock+C57BL/6-Clock

behavior/neurological phenotype

Genotype: Clockm1Jt/Clockm1JtC57BL/6J-Clock/J

digestive/alimentary phenotype

homeostasis/metabolism phenotype

Genotype: Clockm1Jt/Clockm1Jtinvolves: C57BL/6J

cellular phenotype

homeostasis/metabolism phenotype

endocrine/exocrine gland phenotype

Genotype: Clockm1Jt/Clockm1JtC57BL/6-Clock

adipose tissue phenotype

cardiovascular system phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

liver/biliary system phenotype

behavior/neurological phenotype

Genotype: Clockm1Jt/Clock+B6(C)-Clock

behavior/neurological phenotype

References

Additional References

Additional - Clockm1Jt related

Genotyping Protocols

Breeding Considerations

Citation

Animal Health Reports

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

Live Mouse

Cryorecovery - Pricing

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Additional Use Restrictions Apply

Licensing Information

Clock^m1Jt

Allele Symbol: Clock^m1Jt

Genotype: Clock^m1Jt related

Genotype: Clock^m1Jt/Clock^m1Jt
involves: BALB/c * C57BL/6 * C57BL/6J * Jcl:ICR

Genotype: Clock^m1Jt/Clock^m1Jt
involves: BALB/cJ * C57BL/6

Genotype: Clock^m1Jt/Clock^m1Jt
involves: BALB/cJ * C57BL/6 * C57BL/6J

Genotype: Clock^m1Jt/Clock^m1Jt
involves: C57BL/6 * Jcl:ICR

Genotype: Clock^m1Jt/Clock^m1Jt
involves: C57BL/6 * C57BL/6J * Jcl:ICR

Genotype: Clock^m1Jt/Clock⁺ Usf1^soc/Usf1⁺
(BALB/cJ x C57BL/6J)F1

Genotype: Clock^m1Jt/Clock⁺ Usf1^soc/Usf1^soc
C.B6-Clock

Genotype: Clock^m1Jt/Clock⁺
involves: C57BL/6

Genotype: Clock^m1Jt/Clock^m1Jt
involves: C57BL/6

Genotype: Clock^m1Jt/Clock^m1Jt
involves: C57BL/6 * C57BL/6J

Genotype: Clock^m1Jt/Clock⁺
C57BL/6-Clock

Genotype: Clock^m1Jt/Clock^m1Jt
C57BL/6J-Clock/J

Genotype: Clock^m1Jt/Clock^m1Jt
involves: C57BL/6J

Genotype: Clock^m1Jt/Clock^m1Jt
C57BL/6-Clock

Genotype: Clock^m1Jt/Clock⁺
B6(C)-Clock

Additional - Clock^m1Jt related