C57BLKS/J is closely related to C57BL/6J, but the strains are phenotypically distinct. Differences include more severe diet-induced atherosclerotic lesions in C57BLKS/J mice, low total cholesterol and low HDL cholesterol when fed a normal diet, and high total cholesterol and HDL cholesterol in an atherogenic diet. C57BLKS/J mice have a relatively high percentage of reticulocytes per total number of erythrocytes, high white blood cell count per volume, with a high percentage of lymphocytes and basophils and a low percentage of neutrophils per total number of leukocytes. C57BLKS/J mice exhibit age related hearing loss.Read More +
This strain is homozygous for Cdh23ahl, the age related hearing loss 1 mutation, which on this background results in progressive hearing loss with onset prior to three months of age.
Although C57BLKS/J is estimated to have more than 70% of its genome derived from C57BL/6J, these strains are phenotypically distinct. Diet-induced atherosclerotic lesions are much more severe in C57BLKS/J than in C57BL/6J or many other inbred strains. Compared with a panel of inbred strains, C57BLKS/J was found to have low total cholesterol and low HDL cholesterol when fed a normal diet and high total cholesterol and HDL cholesterol in an atherogenic diet. Paigen et al. found high levels of plasma bile salts in C57BLKS/J females after eight weeks on an atherogenic diet. The mutations diabetes (Leprdb) and obese (Lepob) each express a much more severe phenotype on the C57BLKS/J background than on the C57BL/6J background. The Cpefat mutation causes severe obesity, hyperinsulinemia, and hyperglycemia on the C57BLKS/J background rather than the hyperinsulinemia, and mild obesity without hyperglycemia found on the HRS/J background. In a comparative study of 43 inbred strains, Barker and Peters found that C57BLKS/J had a relatively high percentage of reticulocytes per total number of erythrocytes, high white blood cell count per volume, with a high percentage of lymphocytes and basophils and a low percentage of neutrophils per total number of leukocytes. C57BLKS/J mice exhibit age related hearing loss by three months of age.
In October, 1947, while at The Sloan-kettering Institute, Dr. N. Kaliss obtained a C57BL/6J male from The Jackson Laboratory and obtained a female, which was reported to be one generation removed from the male, from a pen-bred colony of C57BL/6J of Dr. J. J. Biesele. Dr. Kaliss bred these together and maintained an inbreeding line of what he thought were C57BL/6J and brought them back with him to The Jackson Laboratory in 1948. He found that with continued inbreeding this strain rejected the C57BL/6-derived sarcoma E0771. It was subsequently determined that this strain had a genetic contamination untraced in origin. Rather than the H2b of C57BL/6J, this strain was found homozygous for the H2d haplotype found also in DBA/2J. Polymorphisms have been assessed to characterize this contamination and Mao et al., following on work of Naggert et al. and Slingsby et al., reported finding that the C57BLKS/J genome derived from 71% C57BL/6J, 25% DBA/2J, and 4% from a combination of C57BL/10J, a 129 source, and possibly some other undefined source. Clusters of 129-like alleles were found on Chr 4 and 15, C57BL/10-like alleles were found on Chr 11 and elsewhere in the genome, and additional unique alleles were also identified.
|Allele Name||age related hearing loss 1|
|Allele Synonym(s)||age related hearing loss 1; Cdh23ahl|
|Gene Symbol and Name||Cdh23, cadherin 23 (otocadherin)|
|Gene Synonym(s)||bob; bustling; bobby; nmf112; nmf252; nmf252; 4930542A03Rik; ahl; 4930542A03Rik; W; sals; mdfw; neuroscience mutagenesis facility, 181; neuroscience mutagenesis facility, 252; modifier of deaf waddler; age related hearing loss 1; v; USH1D; nmf181; RIKEN cDNA 4930542A03 gene; CDHR23; sals; waltzer; nmf112; nmf181; mdfw; neuroscience mutagenesis facility, 112; bus; ahl; bob; salsa; PITA5|
|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: CD-1, 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.|
|Allele Name||b-1 variant|
|Allele Type||Not Applicable|
|Allele Synonym(s)||Ahrb-1; b-1 variant|
|Gene Symbol and Name||Ahr, aryl-hydrocarbon receptor|
|Gene Synonym(s)||bHLHe76; aromatic hydrocarbon responsiveness; aryl hydrocarbon hydroxylase; Ahh; dioxin receptor; In; Ah; Ahre; inflammatory reactivity; RP85|
|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.|
When using the C57BLKS/J mouse strain in a publication, please include JAX stock #000662 in your Materials and Methods section.
|Inbred, 1 pair minimum will be supplied|
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.
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