Overview

This strain carries the Clock (circadian locomotor output cycles kaput) delta 19 ENU mutation on a BALB/cJ genetic background. This strain may be useful in studies of circadian rhythm.

Donating Investigator

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

Genetic overview

Genetic Background	Generation

Clock^m1Jt

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

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Research Applications

Reproductive Biology Research
Neurobiology Research

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

This strain carries the delta 19 Clock (circadian locomotor output cycles kaput) mutation on a BALB/cJ genetic background. As compared with the original C57BL/6 background see Stock No. 002923), the circadian phenotype of BALB/c animals is suppressed. Heterozygotes and homozygotes are viable and fertile.

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) were originally maintained on the C57BL/6J genetic background (see Stock No. 002923). This Clock^delta19 strain has been backcrossed to BALB/cJ for more than 10 generations by the donating laboratory.

Control Suggestions

+/+ from the colony

Approximate Controls

000651 BALB/cJ

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

View All References

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

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

Neurobiology Research
- Circadian Rhythms

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⁺
C57BL/6-Clock

behavior/neurological phenotype

abnormal behavior
- Normal - however, anxiety and depressive-like behavior are not increased
- in a forced-swim test, female mice exhibit less immobility compared with wild-type mice but as much as in Clock^m1Jt homozygotes

abnormal sleep pattern
- during the 12 hour dark phase, REM sleep is shorter than in 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, mice spend less time in non-REM sleep than 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

prolonged circadian behavior 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
- increased 0.6 hr upon exposure to constant darkness
- 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 vertical activity
- in female mice in an open field test

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

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

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

behavior/neurological phenotype

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

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

behavior/neurological phenotype

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

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

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

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 circadian behavior phase
- 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
- 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
- in constant darkness, mice exhibit a 3 to 4 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
- in an elevated plus maze, female mice exhibit increased number of arm entries compared with wild-type mice

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

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

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

hyperactivity
- during the light phase
- in female mice

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

cardiovascular system phenotype

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

decreased heart rate
- only during the active phase

abnormal circadian regulation of systemic arterial blood pressure
- diurnal variation in mean arterial pressure is disrupted during the light 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 circulating triglyceride level
- at 6 to 7 months when fed a regular diet

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

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 leptin level
- during the light phase when fed a regular and during the light and dark phase when fed a high fat diet

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

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

liver/biliary system phenotype

hepatic steatosis
- when fed a high fat diet

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

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

integument phenotype

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

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

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

homeostasis/metabolism phenotype

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

mammalian phenotype

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

behavior/neurological phenotype

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

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

abnormal sleep pattern
- mice spend less time in non-REM sleep with an increase in waking compared with 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
- peak electroencephalogram delta power of non-REM sleep appears at the onset of the light period unlike in wild-type mice

hyperactivity
- in an open field test

increased vertical activity
- in an open field test

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

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

homeostasis/metabolism phenotype

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

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

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

digestive/alimentary phenotype

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

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

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

decreased 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
- islets from young mice show impaired glucose-stimulated insulin secretion

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

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
- 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
- 23% decrease in proliferation of islets
- islets lack a circadian rhythm, even after forskolin stimulation

decreased 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 from young mice show impaired glucose-stimulated insulin secretion
- islets display diminished insulin secretory responses to the cyclase activators forskolin and exendin 4, and 8-bromo-cAMP

small pancreatic islets

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

increased pancreatic islet cell apoptosis
- trend toward increased islet apoptosis

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

homeostasis/metabolism phenotype

decreased physiological sensitivity to xenobiotic
- Normal - however, kaolin-induced bradykinin production and blood pressure suppression are normal
- kaolin-induced writhing day-night fluctuations are abolished and writhing is decreased during the inactive phase compared to in similarly treated wild-type mice

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

nervous system phenotype

abnormal medium spiny neuron morphology
- lithium treatment reverses the changes in dendritic morphology
- nucleus accumbens medium spiny neurons have longer and more complex dendrites and exhibit reduced GluR1 expression than those of wild-type mice

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: 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: C57BL/6

homeostasis/metabolism phenotype

abnormal luteinizing hormone level
- 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
- mice fail to exhibit an increase in luteinizing hormone level on the day of proestrus unlike wild-type mice

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

abnormal lipid homeostasis
- diurnal variation in triglyceride levels is disrupted

decreased circulating luteinizing hormone level
- 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 circulating progesterone level
- during proestrus

increased circulating estradiol level
- during proestrus

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

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

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

impaired gluconeogenesis

increased circulating progesterone 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

prolonged estrus

short proestrus

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

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 estrous cycle

behavior/neurological phenotype

increased vertical activity
- in a novel environment

hyperactivity
- in a novel environment

prolonged circadian behavior period

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

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

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

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

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

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 - Clock^m1Jt related

Technical Support

CONTACT TECHNICAL SUPPORT

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

When maintained as a live colony, heterozygotes or homozygotes may be bred.
- Additional Breeding and Husbandry Support
Citation
When using the C.B6-Clock^m1Jt/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #016175 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
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

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

Related Products and Services

Frozen Mouse Embryo	C.B6-Clock<m1Jt>/J	$2595.00
Frozen Mouse Embryo	C.B6-Clock<m1Jt>/J	$2595.00
Frozen Mouse Embryo	C.B6-Clock<m1Jt>/J	$3373.50
Frozen Mouse Embryo	C.B6-Clock<m1Jt>/J	$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

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Approximate Controls

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/Clock+C57BL/6-Clock

behavior/neurological phenotype

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

behavior/neurological phenotype

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

behavior/neurological phenotype

Genotype: Clockm1Jt/Clockm1JtC57BL/6-Clock

adipose tissue phenotype

behavior/neurological phenotype

cardiovascular system phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

liver/biliary system phenotype

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

behavior/neurological phenotype

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

integument phenotype

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

homeostasis/metabolism phenotype

mammalian phenotype

behavior/neurological phenotype

Genotype: Clockm1Jt/Clock+involves: C57BL/6

homeostasis/metabolism 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/Clockm1Jtinvolves: BALB/c * C57BL/6 * C57BL/6J * Jcl:ICR

homeostasis/metabolism phenotype

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

nervous system phenotype

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

behavior/neurological phenotype

mammalian phenotype

Genotype: Clockm1Jt/Clockm1Jtinvolves: C57BL/6

homeostasis/metabolism phenotype

mammalian phenotype

nervous system phenotype

reproductive system phenotype

behavior/neurological phenotype

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

mammalian phenotype

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⁺
C57BL/6-Clock

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Additional - Clock^m1Jt related