JAX Mouse Strain Datasheet - 002923

C57BL/6J-Clock^m1Jt/J

Stock No:: 002923 |; Clock

Cryo Recovery

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:

$2,595.00 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):719-25. PubMed: 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)	5330400M04Rik; 5330400M04Rik; KAT13D; RIKEN cDNA 5330400M04 gene; bHLHe8; mKIAA0334
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

Research Areas By Genotype

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

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

behavior/neurological phenotype

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

abnormal sleep pattern
- during the 12 hour dark phase, REM sleep is shorter than in wild-type mice
- 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

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

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

prolonged circadian 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
- 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

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

behavior/neurological phenotype

abnormal circadian rhythm
- diurnal variations in thrombotic vascular occlusion subsequent to photochemical injury observed in similarly treated wild-type mice

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

behavior/neurological phenotype

prolonged circadian 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^m1Jt
C57BL/6-Clock^m1Jt

behavior/neurological phenotype

abnormal behavior
- 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 circadian 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
- in constant darkness, mice exhibit a 3 to 4 hour increase in free-running rhythm of locomotor activity compared with 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

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

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

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

abnormal locomotor activation
- activity levels are 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
- during the 12 hour dark phase, REM sleep is longer 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
- during the 12 hour light phase, sleep episodes are shorter 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
- mice spend 18% less time asleep during the entire 24 hour light dark cycle compared with 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

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

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

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

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

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

decreased circulating corticosterone level

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

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

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

adipose tissue phenotype

increased fat cell size
- when fed a high fat diet

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

growth/size/body region phenotype

increased body weight
- when fed a regular or 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

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

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

digestive/alimentary phenotype

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

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

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

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/6

homeostasis/metabolism phenotype

abnormal gluconeogenesis
- impaired

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

abnormal luteinizing hormone level
- estradiol benzoate-injected mice fail to exhibit a surge in luteinizing hormone unlike similarly treated wild-type mice
- 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

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

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

decreased circulating progesterone level
- during proestrus

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

increased circulating estradiol level
- during proestrus

increased circulating progesterone level
- during proestrus

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

behavior/neurological phenotype

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

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

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

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

hyperactivity
- in a novel environment

increased vertical activity
- in a novel environment

prolonged circadian period

reproductive system phenotype

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

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

prolonged estrous cycle

prolonged estrus

reproductive system phenotype
- ovarian tissue morphology is normal

short proestrus

nervous system phenotype

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

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^m1Jt
involves: C57BL/6J

endocrine/exocrine gland phenotype

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

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

decreased insulin secretion
- islets display diminished insulin secretory responses to the cyclase activators forskolin and exendin 4, and 8-bromo-cAMP
- 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

increased pancreatic islet cell apoptosis
- trend toward increased islet apoptosis

small pancreatic islets

homeostasis/metabolism phenotype

decreased insulin secretion
- islets display diminished insulin secretory responses to the cyclase activators forskolin and exendin 4, and 8-bromo-cAMP
- 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

hyperglycemia
- 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
- 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

impaired glucose 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
- however, mice show normal insulin tolerance

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

insulin resistance
- gradual onset of insulin resistance

behavior/neurological phenotype

abnormal circadian rhythm
- 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

cellular phenotype

increased pancreatic islet cell apoptosis
- trend toward increased islet apoptosis

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

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

behavior/neurological phenotype

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

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

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

behavior/neurological phenotype

abnormal circadian rhythm
- however, entrainment is intact
- peak electroencephalogram delta power of non-REM sleep appears at the onset of the light period unlike in wild-type mice
- the acrophase of REM sleep is delayed 4.4 hours compared to in wild-type mice
- the acrophase of body temperature, spontaneous activity, and sleep are delayed 2 to 3 hours compared to in wild-type mice
- the acrophases of body temperature, spontaneous activity, and wake are 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

abnormal circadian temperature homeostasis
- during the first half of the dark period and at the end of the light period

abnormal sleep pattern
- 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 acrophase of REM sleep is delayed 4.4 hours compared to 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

behavior/neurological phenotype
- mice exhibit normal passive avoidance

hyperactivity
- in an open field test

increased vertical activity
- in an open field test

homeostasis/metabolism phenotype

abnormal circadian temperature homeostasis
- during the first half of the dark period and at the end of the light period

Genotype: Clock^m1Jt/Clock^m1Jt
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

homeostasis/metabolism phenotype

decreased physiological sensitivity to xenobiotic
- 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
- 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
- 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

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

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

nervous system phenotype

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

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

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

behavior/neurological phenotype

prolonged circadian 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^m1Jt

behavior/neurological phenotype

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

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

Additional - Clock^m1Jt related

Ando N; Nakamura Y; Aoki R; Ishimaru K; Ogawa H; Okumura K; Shibata S; Shimada S; Nakao A. 2015. Circadian Gene Clock Regulates Psoriasis-Like Skin Inflammation in Mice. J Invest Dermatol 135(12):3001-8. PubMed: 26291684 MGI: J:227724
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: 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: J:166003
Antoch MP; Gorbacheva VY; Vykhovanets O; Toshkov IA; Kondratov RV; Kondratova AA; Lee C; Nikitin AY. 2008. Disruption of the circadian clock due to the Clock mutation has discrete effects on aging and carcinogenesis. Cell Cycle 7(9):1197-204. PubMed: 18418054 MGI: J:224359
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: 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: 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: J:135812
Casey T; Crodian J; Suarez-Trujillo A; Erickson E; Weldon B; Crow K; Cummings S; Chen Y; Shamay A; Mabjeesh SJ; Plaut K. 2016. CLOCK regulates mammary epithelial cell growth and differentiation. Am J Physiol Regul Integr Comp Physiol 311(6):R1125-R1134. PubMed: 27707717 MGI: J:242653
Challet E; Takahashi JS; Turek FW. 2000. Nonphotic phase-shifting in clock mutant mice. Brain Res 859(2):398-403. PubMed: 10719095 MGI: J:61117
Cordes S; Gallistel CR. 2008. Intact interval timing in circadian CLOCK mutants. Brain Res 1227:120-7. PubMed: 18602902 MGI: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: J:185630
He B; Nohara K; Park N; Park YS; Guillory B; Zhao Z; Garcia JM; Koike N; Lee CC; Takahashi JS; Yoo SH; Chen Z. 2016. The Small Molecule Nobiletin Targets the Molecular Oscillator to Enhance Circadian Rhythms and Protect against Metabolic Syndrome. Cell Metab 23(4):610-21. PubMed: 27076076 MGI: J:235403
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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: J:131221
Kyoko OO; Kono H; Ishimaru K; Miyake K; Kubota T; Ogawa H; Okumura K; Shibata S; Nakao A. 2014. Expressions of tight junction proteins Occludin and Claudin-1 are under the circadian control in the mouse large intestine: implications in intestinal permeability and susceptibility to colitis. PLoS One 9(5):e98016. PubMed: 24845399 MGI: J:216525
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: J:151782
Liu J; Zhou B; Yan M; Huang R; Wang Y; He Z; Yang Y; Dai C; Wang Y; Zhang F; Zhai Q. 2016. CLOCK and BMAL1 Regulate Muscle Insulin Sensitivity via SIRT1 in Male Mice. Endocrinology 157(6):2259-69. PubMed: 27035655 MGI: J:234964
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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: J:147996
Nakamura T; Takumi T; Takano A; Hatanaka F; Yamamoto Y. 2013. Characterization and modeling of intermittent locomotor dynamics in clock gene-deficient mice. PLoS One 8(3):e58884. PubMed: 23516567 MGI: J:200187
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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: J:153782
Pan X; Jiang XC; Hussain MM. 2013. Impaired cholesterol metabolism and enhanced atherosclerosis in clock mutant mice. Circulation 128(16):1758-69. PubMed: 24014832 MGI: J:218726
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: 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: 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: J:109337
Podobed PS; Alibhai FJ; Chow CW; Martino TA. 2014. Circadian regulation of myocardial sarcomeric Titin-cap (Tcap, telethonin): identification of cardiac clock-controlled genes using open access bioinformatics data. PLoS One 9(8):e104907. PubMed: 25121604 MGI: J:218985
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: J:147991
Ripperger JA; Jud C; Albrecht U. 2011. The daily rhythm of mice. FEBS Lett 585(10):1384-92. PubMed: 21354419 MGI: 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: 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: 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: 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: J:145372
Sei H; Oishi K; Morita Y; Ishida N. 2001. Mouse model for morningness/eveningness. Neuroreport 12(7):1461-4. PubMed: 11388430 MGI: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: J:198493

Also Known As: Clock

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Clockm1Jt

Allele Symbol: Clockm1Jt

Disease Terms

Research Areas By Genotype

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-Clockm1Jt

behavior/neurological phenotype

Genotype: Clockm1Jt/Clock+involves: C57BL/6

homeostasis/metabolism phenotype

behavior/neurological phenotype

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

behavior/neurological phenotype

Genotype: Clockm1Jt/Clockm1JtC57BL/6-Clockm1Jt

behavior/neurological phenotype

homeostasis/metabolism phenotype

cardiovascular system phenotype

adipose tissue phenotype

growth/size/body region phenotype

liver/biliary system phenotype

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

digestive/alimentary phenotype

homeostasis/metabolism phenotype

Genotype: Clockm1Jt/Clockm1Jtinvolves: C57BL/6

homeostasis/metabolism phenotype

behavior/neurological phenotype

reproductive system phenotype

nervous system phenotype

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

integument phenotype

Genotype: Clockm1Jt/Clockm1Jtinvolves: C57BL/6J

endocrine/exocrine gland phenotype

homeostasis/metabolism phenotype

behavior/neurological phenotype

cellular phenotype

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

behavior/neurological phenotype

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

behavior/neurological phenotype

homeostasis/metabolism phenotype

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

behavior/neurological phenotype

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

nervous system phenotype

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

behavior/neurological phenotype

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

behavior/neurological phenotype

References

Additional References

Additional - Clockm1Jt related

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

Live Mouse

Cryorecovery - Pricing

Progeny testing is not required

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Clock^m1Jt

Allele Symbol: Clock^m1Jt

Genotype: Clock^m1Jt related

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

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

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

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

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

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

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

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

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

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

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⁺ Usf1^soc/Usf1⁺
(BALB/cJ x C57BL/6J)F1

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

Additional - Clock^m1Jt related