JAX Mouse Strain Datasheet - 016175

C.B6-Clock^m1Jt/J

Stock No:: 016175

Cryo Recovery

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

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

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.. In: . . 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:

Neurobiology Research
- Circadian Rhythms

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⁺ 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

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^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 behavior 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 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
- 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

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

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^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 behavior
- 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 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 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
- 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 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

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

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

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 behavior 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
involves: C57BL/6 * Jcl:ICR

behavior/neurological phenotype

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

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 REM sleep is delayed 4.4 hours compared to 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

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
- the acrophase of body temperature is delayed by 2 to 3 hours compared with in wild-type mice

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

behavior/neurological phenotype

abnormal circadian behavior
- 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

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
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 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

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

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 behavior 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: 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: C57BL/6J

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

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

cellular phenotype

increased pancreatic islet cell apoptosis
- trend toward increased islet apoptosis

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

behavior/neurological phenotype

arrhythmic circadian behavior 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 behavior 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

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

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

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 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

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.. In: . . MGI: J:18005

Additional - Clock^m1Jt related

Alibhai FJ; Reitz CJ; Peppler WT; Basu P; Sheppard P; Choleris E; Bakovic M; Martino TA. 2017. Female ClockDelta19/Delta19 Mice are Protected from the Development of Age-Dependent Cardiomyopathy.. In: . . MGI: J:243739
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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . MGI: J:242653
Challet E; Takahashi JS; Turek FW. 2000. Nonphotic phase-shifting in clock mutant mice.. In: . . MGI: J:61117
Cordes S; Gallistel CR. 2008. Intact interval timing in circadian CLOCK mutants.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . MGI: J:205653
Doi R; Oishi K; Ishida N. 2010. CLOCK regulates circadian rhythms of hepatic glycogen synthesis through transcriptional activation of Gys2.. In: . . 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.. In: . . 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.. In: . . MGI: J:166742
Easton A; Arbuzova J; Turek FW. 2003. The circadian Clock mutation increases exploratory activity and escape-seeking behavior.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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. In: . . 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.. In: . . 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.. In: . . MGI: J:188150
Kennaway DJ; Boden MJ; Voultsios A. 2004. Reproductive performance in female Clock Delta19 mutant mice.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . MGI: J:40364
Koizumi H; Kurabayashi N; Watanabe Y; Sanada K. 2013. Increased anxiety in offspring reared by circadian Clock mutant mice.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . MGI: J:68852
Malkesman O; Austin DR; Chen G; Manji HK. 2009. Reverse translational strategies for developing animal models of bipolar disorder.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . MGI: J:92343
Mohawk JA; Baer ML; Menaker M. 2009. The methamphetamine-sensitive circadian oscillator does not employ canonical clock genes.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . MGI: J:60291
Oishi K; Koyanagi S; Ohkura N. 2013. The molecular clock regulates circadian transcription of tissue factor gene.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . MGI: J:203608
Pan X; Hussain MM. 2009. Clock is important for food and circadian regulation of macronutrient absorption in mice.. In: . . MGI: J:153782
Pan X; Jiang XC; Hussain MM. 2013. Impaired cholesterol metabolism and enhanced atherosclerosis in clock mutant mice.. In: . . 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.. In: . . 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.. In: . . MGI: J:209595
Pitts S; Perone E; Silver R. 2003. Food-entrained circadian rhythms are sustained in arrhythmic Clk/Clk mutant mice.. In: . . 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.. In: . . 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.. In: . . MGI: J:147991
Ripperger JA; Jud C; Albrecht U. 2011. The daily rhythm of mice.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . MGI: J:145372
Sei H; Oishi K; Morita Y; Ishida N. 2001. Mouse model for morningness/eveningness.. In: . . 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.. In: . . 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.. In: . . 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]. In: . . MGI: J:62075
Shearman LP; Weaver DR. 1999. Photic induction of Period gene expression is reduced in Clock mutant mice.. In: . . 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.. In: . . 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.. In: . . MGI: J:198519
Shostak A; Meyer-Kovac J; Oster H. 2013. Circadian regulation of lipid mobilization in white adipose tissues.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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.. In: . . 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. In: . . 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.. In: . . 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.. In: . . MGI: J:198493

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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+ Usf1soc/Usf1socC.B6-Clockm1Jt

behavior/neurological phenotype

Genotype: Clockm1Jt/Clock+C57BL/6-Clockm1Jt

behavior/neurological phenotype

Genotype: Clockm1Jt/Clock+involves: C57BL/6

homeostasis/metabolism 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/Clockm1Jtinvolves: C57BL/6 * Jcl:ICR

behavior/neurological phenotype

homeostasis/metabolism phenotype

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

behavior/neurological 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: BALB/cJ * C57BL/6 * C57BL/6J

nervous system phenotype

Genotype: Clockm1Jt/Clockm1Jtinvolves: C57BL/6J

endocrine/exocrine gland phenotype

homeostasis/metabolism phenotype

cellular phenotype

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

behavior/neurological phenotype

nervous system phenotype

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

homeostasis/metabolism phenotype

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

behavior/neurological phenotype

References

Additional - Clockm1Jt related

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Clock^m1Jt

Allele Symbol: Clock^m1Jt

Genotype: Clock^m1Jt related

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

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
involves: C57BL/6 * Jcl:ICR

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

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: BALB/cJ * C57BL/6 * C57BL/6J

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

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

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

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

Additional - Clock^m1Jt related