C57BL/6J is the most widely used inbred strain and the first to have its genome sequenced. Although this strain is refractory to many tumors, it is a permissive background for maximal expression of most mutations. C57BL/6J mice are resistant to audiogenic seizures, have a relatively low bone density, and develop age related hearing loss. They are also susceptible to diet-induced obesity, type 2 diabetes, and atherosclerosis. Macrophages from this strain are resistant to the effects of anthrax lethal toxin.
Study-ready aged C57BL/6J males and females between 25 - 78 weeks of age available for order.
This strain is homozygous for Cdh23ahl, the age related hearing loss 1 mutation, which on this background results in progressive hearing loss with onset after 10 months of age.
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) portosystemic shunts (~5%); 7) hairloss associated with overgrooming, 8) a preference for alcohol and morphine; 9) late-onset hearing loss; and 10) 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. Cheers and McKenzie found C57BL/6J resistant to listeriosis. 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-Tr20m1J 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).
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.
|Allele Name||b-1 variant|
|Allele Type||Not Applicable|
|Allele Synonym(s)||Ah; Ahb-1; Ahb; Ahhi; Ahrb; In|
|Gene Symbol and Name||Ahr, aryl-hydrocarbon receptor|
|Gene Synonym(s)||Ah; Ahh; Ahre; In; aromatic hydrocarbon responsiveness; aryl hydrocarbon hydroxylase; bHLHe76; dioxin receptor; inflammatory reactivity|
|Strain of Origin||C57BL/6J|
|General Note||C57BL/6 carries the responsive Ahrb allele; DBA/2 carries nonresponsive Ahrd. Heterozygotes (Ahrb/Ahrd) are responsive (J:5282). Later work identified a second (J:8895) and later a third (J:22144) allele conferring response. Thus the allele in C57, C58, and MA/My strains is now Ahrb-1; Ahrb-2 is carried by BALB/cBy, A, and C3H; and Ahrb-3 by Mus spretus, M. caroli, and MOLF/Ei. The nonresponsive strains AKR, DBA/2, and 129 carry Ahrd (J:22144). Nucleotide and amino acid sequence differences between Ahrb-1 and Ahrd have been determined (J:17460). |
Strain of origin - this allele was found in C57BL/6, C58/J, C57BR, MA/My strains
|Molecular Note||This allele encodes a high affinity, relatively heat stabile, 95 kDa receptor. PCR sequencing of cDNA revealed ten nucleotide differences between the coding sequences of the DBA/2J and C57BL/6J receptors. Five of the ten differences would cause amino acid changes. One of these, a C to T transition in exon 11 would change the arginine codon in the DBA/2J allele to an opal termination codon in the C57BL/6J allele. This change would prevent the 43 amino acid extension of mRNA translation predicted for the DBA/2J allele and account for the smaller size of the peptide produced by this allele (95 kDa vs 104 kDa for the DBA/2J allele). A second C to T transition changes a proline codon in the DBA/2J allele to leucine codon in the C57BL/6J allele, and would likely change secondary structure of the peptide and thus ligand affinity.|
|Allele Name||age related hearing loss 1|
|Allele Synonym(s)||Cdh23753A; mdfw|
|Gene Symbol and Name||Cdh23, cadherin 23 (otocadherin)|
|Gene Synonym(s)||4930542A03Rik; 4930542A03Rik; CDHR23; PITA5; RIKEN cDNA 4930542A03 gene; USH1D; W; age related hearing loss 1; ahl; ahl; bob; bob; bobby; bus; bustling; mdfw; mdfw; modifier of deaf waddler; neuroscience mutagenesis facility, 112; neuroscience mutagenesis facility, 181; neuroscience mutagenesis facility, 252; nmf112; nmf112; nmf181; nmf181; nmf252; nmf252; sals; sals; salsa; v; waltzer|
|Strain of Origin||multiple strains|
|Molecular Note||Genetic complementation tests have shown allelism between the mdfw (modifier of deaf waddler) locus and the ahl locus. Further analysis has shown this is caused by a G to A transition at nucleotide position 753 of Cdh23. This hypomorphic allele causes in frame skipping of exon 7, which is predicted to delete part of the 2nd and 3rd ectodomains, and cause reduced message stability. Twenty-seven strains classified with ahl and carrying the 753A allele include: CD1, RBF/DnJ, PL/J, AKR/J, RF/J, BALB/cBy, A/WySnJ, P/J, SENCARA/PtJ, DBA/1J, ALS/LtJ, C58/J, C57BLKS/J, 129P1/ReJ, C57BR/cd, SKH2/J, BUB/Bn, MA/MyJ, LP/J, 129X1/SvJ, NOR/LtJ, A/J, C57BL/6, NOD/LtJ, DBA/2J, ALR/LtJ, C57L/J. Strains classified with ahl that DO NOT carry this mutation include: C3H/HeSnJ, I/LnJ, YBR/Ei, MRL/MpJ.|
|Gene Symbol and Name||Gluchos3, glucose homeostasis QTL 3|
|Strain of Origin||C57BL/6J|
|Molecular Note||This allele confers 50% decreased plasma insulin at T30 during the intraperitoneal glucose tolerance test compared to C3H/HeH.|
|Gene Symbol and Name||Micrl, microwave induced increase in complement receptor B cells|
|Strain of Origin||multiple strains|
|General Note||The following inbred strains are homozygous for the recessive QTL, Micrl |
|Allele Type||Spontaneous (Not Applicable)|
|Gene Symbol and Name||Nlrp12, NLR family, pyrin domain containing 12|
|Gene Synonym(s)||CLR19.3; FCAS2; NACHT, LRR and PYD containing protein 12; NALP12; Nalp12; Nalp12; PAN6; PYPAF7; RNO; RNO2|
|Strain of Origin||C57BL/6J|
|Molecular Note||A sequence variant is identified in C57BL/6J (T) as compared to C57BL/6N (C) at position 3,222,538 (version mm9-NCB1m37). The polymorphism is located in the C-terminal leucine-rich repeat domain and results in a arginine to lysine change at amino acid residue 1034.|
|Gene Symbol and Name||Nnt, nicotinamide nucleotide transhydrogenase|
|Gene Synonym(s)||4930423F13Rik; 4930423F13Rik; AI323702; BB168308; GCCD4; RIKEN cDNA 4930423F13 gene; expressed sequence AI323702; expressed sequence BB168308|
|Strain of Origin||C57BL/6J|
|Molecular Note||This allele contains a stretch of 17,814 bp missing between exons 6 and 12. RT-PCR demonstrated cDNA corresponding to exons 7-11 was absent. Mature protein was not detected in these mutants.|
|Gene Symbol and Name||P2rx7, purinergic receptor P2X, ligand-gated ion channel, 7|
|Gene Synonym(s)||AI467586; P2X(7); P2X7; P2X7 receptor; P2X7R; expressed sequence AI467586|
|Strain of Origin||various|
|Molecular Note||A proline to leucine change at amino acid residue 451 is caused by a T to C transition at nucleic acid base 1352. This mutation is found in C57BL/6, C57BL/10, DBA/1, and DBA/2 and contrasts with the condition in BALB/c, NZW, NOD, 129, Mus caroli, M. spretus, M. musculus, and M. poschiavinus. The mutation lies within a C-terminal cytoplasmic domain homologous with the TNFR 1-death domain and with an SH3 binding protein.|
|Allele Name||mutation 1, Jackson|
|Allele Type||Spontaneous (Not Specified)|
|Allele Synonym(s)||n-TRtct5rs4644711-T; n-Tr20C57BL/6J; rs46447118|
|Gene Symbol and Name||n-TRtct5, nuclear encoded tRNA arginine 5 (anticodon TCT)|
|Gene Synonym(s)||n-Tr20; nuclear encoded tRNA arginine 20 (anticodon TCT); trna730-ArgTCT|
|Strain of Origin||C57BL/6J|
|Molecular Note||This C to T transition, found in C57BL/6J and C57BL/6JEiJ but not other inbred strains, is in nucleotide 50 in the stem of the T loop and impairs maturation, leading to accumulation of a 105 nucleotide pre-tRNA band with leader and trailer sequences instead of the usual 115 nucleotide pre-tRNA, and also diminishes aminoacylation of this isodecoder.|
When using the Black 6 mouse strain in a publication, please include JAX stock #000664 in your Materials and Methods section.
Volume Pricing Program
Quantities: Volume pricing is automatically applied when a minimum quantity per strain for a shipment is reached
Sexes: Sexes of the same strain may be combined to reach minimum quantity levels to receive the volume pricing
Shipment: All shipping destinations qualify
This strain is available from some international Charles River (CR) breeding facilities in Japan and/or Europe. For more information, see the Worldwide Distributor List for JAX® Mice.
We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.
Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation.
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