Type: Inbred Strain;

Additional information on Inbred Strains.

Visit the JAX^® online Nomenclature tutorial.

Mating System: Sibling x Sibling         (Female x Male)   01-MAR-06

Breeding Considerations: This strain is a good breeder.

Species: laboratory mouse

H2 Haplotype: b

Generation: F226pF230 (14-AUG-14)

Generation Definitions

 

Appearance

black
Related Genotype: a/a

Important Note

This strain is homozygous for Cdh23^ahl, the age related hearing loss 1 mutation, which on this background results in progressive hearing loss with onset after 10 months of age.

Description

C57BL/6 is the most widely used inbred strain. It is commonly used as a general purpose strain and background strain for the generation of congenics carrying both spontaneous and induced mutations. Although this strain is refractory to many tumors, it is a permissive background for maximal expression of most mutations. C57BL/6J mice are used in a wide variety of research areas including cardiovascular biology, developmental biology, diabetes and obesity, genetics, immunology, neurobiology, and sensorineural research. C57BL/6J mice are also commonly used in the production of transgenic mice. Overall, C57BL/6 mice breed well, are long-lived, and have a low susceptibility to tumors. Primitive hematopoietic stem cells from C57BL/6J mice show greatly delayed senescence relative to BALB/c and DBA/2J. This is a dominant trait. Other characteristics include: 1) a high susceptibility to diet-induced obesity, type 2 diabetes, and atherosclerosis; 2) a high incidence of microphthalmia and other associated eye abnormalities; 3) resistance to audiogenic seizures; 4) low bone density; 5) hereditary hydrocephalus (early reports indicate 1 – 4 %); 6) hairloss associated with overgrooming, 7) a preference for alcohol and morphine; 8) late-onset hearing loss; and 9) increased incidence of hydrocephalus and malocclusion.

C57BL/6J mice fed a high-fat diet develop obesity, mild to moderate hyperglycemia, and hyperinsulinemia (see JAX^® Diet-induced Obesity (DIO) Models). C57BL/6J mice fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat) for 14 weeks develop lesions in the range of 4500 to 8000 um² atherosclerotic aortic lesions/aortic cross-section. The variation in aortic lesions found among various inbred strains has led to the identification of the existence of eight genes affecting atherosclerosis, Ath1 to Ath8. C57BL/6J mice also develop severe and progressive hearing loss later in life. Histopathological changes associated with age-related hearing loss include the disruption of both outer and inner hair cells. C57BL/6 mice are also more susceptible to noise-induced hearing loss. Age related hearing loss 1 (Ahl), a major gene responsible for this hearing loss, was mapped in an intersubspecific backcross by measuring elevated auditory-evoked brainstem response (ABR) thresholds. Ahl is located on Chromosome 10 near marker D10Mit5. A naturally occurring deletion in nicotinamide nucleotide transhydrogenase (Nnt) exons 7-11 occurred in C57BL/6J sometime prior to 1984. This deletion results in the absence of the NNT protein, and is associated with impaired glucose homeostasis control and reduced insulin secretion. This mutation is not found in C57BL/6JEi, C57BL/6N, C57BL/6NJ, C57BL/6ByJ, C57BL/10J, C57L/J, or C58/J (Toye AA, et al, Diabetologia, 2005). Since C57BL/6JEi separated from C57BL/6J in 1976, the Nnt deletion arose sometime between 1976 and 1984. Because of the n-Tr20^m1J point mutation, which is also present in C57BL/6JEiJ but not C57BL/6NJ or C57BL/6ByJ, extracts from the cerebellum of C57BL/6J mice have increased ribosomal pausing at AGA codons compared with that of other inbred strains (Ishimura et al., 2014).

C57BL/6J was the DNA source for the international collaboration that generated the first high quality draft sequence of the mouse genome. 5 SNP differences have been identified that distinguish C57BL/6J from C57BL/6ByJ and C57BL/6NJ. Both C57BL/6ByJ and C57BL/6NJ type as follows: 08-015199792-M (rs3709624) is C; 11-004367508-M (rs3659787) is A; 13-041017317-M (rs3722313) is C; 15-057561875-M (rs3702158) is G; 19-049914266-M (rs3724876) is T. C57BL/6J types as follows: 08-015199792-M (rs3709624) is T; 11-004367508-M (rs3659787) is G; 13-041017317-M (rs3722313) is T; 15-057561875-M (rs3702158) is A; 19-049914266-M (rs3724876) is G (Petkov and Wiles, 2004.) Others have subsequently identified further SNP differences between sublines of C57BL/6 (Mekada et al., 2009, Zurita et al., 2010).

Development

The C57BL/6J inbred strain was created by Dr. CC Little from the mating of female 57 with male 52 from Miss Abbie Lathrop’s stock. The same cross gave rise to the C57L and C57BR strains.

 

Additional Web Information

3D MRI Digital Atlas Database of Adult C57BL/6J Mouse Brain
JAX^® NOTES, April 1988; 433. H-2 Haplotypes of Mice from Jackson Laboratory Production Colonies.
JAX^® NOTES, Fall 1995; 463. Inbred C57 Black Mice: Microphthalmia and Ocular Infections.
JAX^® NOTES, Fall 2003; 491. The Importance of Understanding Substrains in the Genomic Age.
JAX^® NOTES, Fall 2006; 503. Cause of Glucose Intolerance in C57BL/6J Mice Discovered.
JAX^® NOTES, Fall 2008; 511. Influence of Nnt alleles on DIO in C57BL/6 JAX^® Mice.
JAX^® NOTES, January 1988; 432. Arthritis Models in the Mouse.
JAX^® NOTES, July 1989; 438. Profile: C57BL/6J.
JAX^® NOTES, October 1987; 431. Alopecia (loss of hair) in C57BL/6J and Related Strains.
JAX^® NOTES, October 1989; 439. Splenic Melanosis in Black Mice.
JAX^® NOTES, Spring 1990; 441. Imperforate Vagina and Mucometra in Mice.
JAX^® NOTES, Spring 2003; 489. Malocclusion in the Laboratory Mouse.
JAX^® NOTES, Spring 2003; 489. Mouse Genome Sequence Released.
JAX^® NOTES, Spring 2004; 493. Chromosome Substitution Strain Panel: A New Tool for Quantitative Trait Loci Analysis.
JAX^® NOTES, Spring 2007; 505. C57BL/6J Strain Used to Construct the Allen Brain Atlas.
JAX^® NOTES, Spring 2009; 513. JAX^® Mice help reveal potential health benefits of resveratrol.
JAX^® NOTES, Summer 1994; 458. Ly5 Gene Nomenclature, C57BL/6J and SJL/J – A History of Change.
JAX^® NOTES, Summer 2003; 490. Charles River Japan Now Breeding JAX^® Mice Strain C57BL/6J.
JAX^® NOTES, Summer 2003; 490. Hydrocephalus in Laboratory Mice.
JAX^® NOTES, Summer 2006; 502. Characterization of DIO Model is Refined.
JAX^® NOTES, Summer 2009; 514. JAX^® Mice Study: Starvation Diet Does Not Extend Life.
JAX^® NOTES, Summer 2009; 514. Another Obesity-modulating Gene Revealed.
JAX^® NOTES, Summer 2009; 514. Defective Gene Plays Unexpected Role in Fat Metabolism.
JAX^® NOTES, Summer 2009; 514. Non-Invasive Technique – Potential Parkinson’s Therapy.
JAX^® NOTES, Winter 2002; 488. Colony Expansions Completed for JAX^® Mice Strains C57BL/6J and BALB/cJ.
JAX^® NOTES, Winter 2006; 504. JAX^® Mice: the Gold Standard Just Got Better.
JAX^® NOTES, Winter 2008; 512. New resource illustrates divergence of C57BL/6 laboratory mouse substrains.
Mouse Phenome Database / SNP Facility
National Center for Biotechnology Information / SNP Data

Please enquire with Customer Service.

Phenotypic Data

Mouse Phenome Database
Festing Inbred Strain Characteristics: C57BL
JAX^® Physiological Data Summary [pdf]
JAX^® Physiological Data Protocol [pdf]

Related Disease (OMIM) Terms provided by MGI

– Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.

Deafness, Autosomal Recessive 12; DFNB12   (CDH23)
Glucocorticoid Deficiency 4; GCCD4   (NNT)
Usher Syndrome, Type ID; USH1D   (CDH23)

Mammalian Phenotype Terms provided by MGI

Assigned by genotype

cardiovascular system phenotype

decreased cardiac muscle contractility

• average left ventricular shortening of 39.1 is significantly lower than the 47.1 in A/J mice   (MGI Ref ID J:76471)
• aortic ejection time is significantly longer than in A/J mice   (MGI Ref ID J:76471)

decreased heart rate

• average 433 beats per minute versus 524 in A/J   (MGI Ref ID J:76471)

increased heart rate

• average heart rate is approximately 50 beats per minute higher than that in A/J   (MGI Ref ID J:76471)

increased left ventricle weight

• average left ventricular weight of 46.2mg is significantly higher than control A/J and results from an increase in the end-diastolic dimension and a proportional increase in wall thickness   (MGI Ref ID J:76471)

muscle phenotype

decreased cardiac muscle contractility

• average left ventricular shortening of 39.1 is significantly lower than the 47.1 in A/J mice   (MGI Ref ID J:76471)
• aortic ejection time is significantly longer than in A/J mice   (MGI Ref ID J:76471)

homeostasis/metabolism phenotype

enhanced exercise endurance

• exercise time on a treadmill is significantly greater than that of A/J   (MGI Ref ID J:76471)

Ahr^b-1/Ahr^b-1

C57BL/6J

mortality/aging

increased sensitivity to xenobiotic induced morbidity/mortality

• mice are susceptible to DMBA induced lethality   (MGI Ref ID J:26440)

homeostasis/metabolism phenotype

*normal* homeostasis/metabolism phenotype

• topical application of the polycyclic hydrocarbon DMBA induced hepatic aryl hydrocarbon hydroxylase activity   (MGI Ref ID J:5387)

• • increased physiological sensitivity to xenobiotic
    • mice are susepctible to the teratogenic effects of TCDD with 100% of mice developing cleft palates and 90% of mice developing severe hydronephrosis   (MGI Ref ID J:132380)
    • mice are susceptible to the pathological effects of DMBA and exhibit lethality, weight loss, peritonitis, decreased spleen weight, and decreased thymus weight   (MGI Ref ID J:26440)
    • mice exposed to DMBA exhibit decreased lymphocyte counts, increased polymorphic cells, decreased bone marrow cell counts and ascites formation   (MGI Ref ID J:26440)
  • increased sensitivity to xenobiotic induced morbidity/mortality
    • mice are susceptible to DMBA induced lethality   (MGI Ref ID J:26440)

immune system phenotype

increased inflammatory response

• topical application of the polycyclic hydrocarbon DMBA produced skin inflammation and ulceration   (MGI Ref ID J:5244)
• topical application of DMBA produced skin inflammation and ulceration   (MGI Ref ID J:5387)

Ahr^b-1/Ahr^b-1

C57BL/6

mortality/aging

increased sensitivity to xenobiotic induced morbidity/mortality

• mice exhibit neonatal lethality in response to in utero exposure to cHBB unlike mice homozygous for the Ahr^d allele   (MGI Ref ID J:113285)

homeostasis/metabolism phenotype

increased physiological sensitivity to xenobiotic

• when mice are fostered by control C57BL/6 dams following in utero exposure to cHBB, 21% of neonates survive   (MGI Ref ID J:113285)
• mice exhibit neonatal lethality in response to in utero exposure to cHBB and decreased thymus and spleen weights compared to untreated mice   (MGI Ref ID J:113285)
• following exposure to cHBB in utero, neonates exhibit an increase in volume density of hematopoietic islands in the liver   (MGI Ref ID J:113285)

• increased sensitivity to xenobiotic induced morbidity/mortality
  • mice exhibit neonatal lethality in response to in utero exposure to cHBB unlike mice homozygous for the Ahr^d allele   (MGI Ref ID J:113285)

Cdh23^ahl/Cdh23^ahl

C57BL/6J

hearing/vestibular/ear phenotype

organ of Corti degeneration

• in 3 of 4 cochleae assesed at 12 months of age the organ of Corti had totally degenerated   (MGI Ref ID J:87783)

nervous system phenotype

cochlear ganglion hypoplasia

• at 9 months of age there is a decrease in the ganglion cell density for each turn over time with the largest cell loss in the basal turn   (MGI Ref IDJ:87783)

Gluchos1^C57BL/6J/Gluchos1^C57BL/6J

C57BL/6J

endocrine/exocrine gland phenotype

decreased insulin secretion

• this phenotype is rescued by transgenic expression of full-length Nnt sequence derived from 129S6/SvEvTac   (MGI Ref ID J:109356)

homeostasis/metabolism phenotype

decreased insulin secretion

• this phenotype is rescued by transgenic expression of full-length Nnt sequence derived from 129S6/SvEvTac   (MGI Ref ID J:109356)

impaired glucose tolerance

• this phenotype is rescued by transgenic expression of full-length Nnt sequence derived from 129S6/SvEvTac   (MGI Ref ID J:109356)

Myo5a^d/Myo5a^d

involves: C57BL/6J

pigmentation phenotype

abnormal melanocyte morphology

• cultured primary melanocytes display clustering of melanosomes but are otherwise normal   (MGI Ref ID J:37976)

Nnt^C57BL/6J/Nnt^C57BL/6J

C57BL/6J

endocrine/exocrine gland phenotype

decreased insulin secretion

• this phenotype is rescued by transgenic expression of full-length Nnt sequence derived from 129S6/SvEvTac   (MGI Ref ID J:109356)

homeostasis/metabolism phenotype

decreased insulin secretion

• this phenotype is rescued by transgenic expression of full-length Nnt sequence derived from 129S6/SvEvTac   (MGI Ref ID J:109356)

impaired glucose tolerance

• this phenotype is rescued by transgenic expression of full-length Nnt sequence derived from 129S6/SvEvTac   (MGI Ref ID J:109356)

P2rx7^P451L/P2rx7^P451L

C57BL/6

cellular phenotype

abnormal cell death

• lysis triggered by extracellular ATP is reduced 45% in C57BL/6 mice as compared to BALB/c   (MGI Ref ID J:89513)

• • abnormal apoptosis
    • sensitivity to extracellular ATP induced apoptosis is reduced in C57BL/6 relative to BALB/c   (MGI Ref ID J:89513)

n-Tr20^m1J/n-Tr20^m1J

C57BL/6J

cellular phenotype

abnormal translational elongation

• compared with C57BL/6J congenic for wildtype n-Tr20 from C57BL/6NJ, extracts from the cerebellum of C57BL/6J inbred mice have more ribosomal pausing at AGA codons and 1.6 times the pausing magnitude at AGA codons   (MGI Ref ID J:211326)

homeostasis/metabolism phenotype

abnormal translational elongation

• compared with C57BL/6J congenic for wildtype n-Tr20 from C57BL/6NJ, extracts from the cerebellum of C57BL/6J inbred mice have more ribosomal pausing at AGA codons and 1.6 times the pausing magnitude at AGA codons   (MGI Ref ID J:211326)

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

Cardiovascular Research
Diet-Induced Atherosclerosis
Susceptible

Developmental Biology Research
Eye Defects
Lymphoid Tissue Defects
hematopoietic defects
Skeletal Defects

Diabetes and Obesity Research
Hyperglycemia
diet-induced, moderate
Hyperinsulinemia
diet-induced
Insulin Resistance
diet-induced
Obesity With Diabetes
diet-induced, moderate
Type 2 Diabetes (NIDDM)
diet-induced

Hematological Research
Hematopoietic Defects

Immunology, Inflammation and Autoimmunity Research
Lymphoid Tissue Defects
hematopoietic development

Neurobiology Research
Behavioral and Learning Defects
Hearing Defects
Age related hearing loss

Research Tools
General Purpose
Genetics Research
Mutagenesis and Transgenesis
Mutagenesis and Transgenesis: Production of Transgenic Mice
Hematological Research
Immunology, Inflammation and Autoimmunity Research
background strain for histocompatibility congenics
Infectious Disease
Salmonella
Tuberculosis (TB)

Sensorineural Research
Eye Defects
Hearing Defects
Age related hearing loss

Ahr^b-1 related

Metabolism Research

Research Tools
Toxicology Research

Cdh23^ahl related

Neurobiology Research
Hearing Defects
Age related hearing loss

Sensorineural Research
Hearing Defects
Age related hearing loss

JAX^® Mice, Products & Services Conditions of Use

“MICE” means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory (“JACKSON”). “PRODUCTS” means biological materials supplied by JACKSON, and their derivatives. “RECIPIENT” means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON’s prior written authorization.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.