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)||Cdh23753A; mdfw|
|Gene Symbol and Name||Cdh23, cadherin 23 (otocadherin)|
|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 coding nucleotide position 753 of Cdh23 (SNP rs257098870). This hypomorphic allele changes splice donor site G-GT to A-GT, causing frame skipping of exon 7. This 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: 129S1/SvImJ, C3H/HeSnJ, I/LnJ, YBR/Ei, MRL/MpJ.|
|Allele Name||b-1 variant|
|Allele Type||Not Applicable|
|Allele Synonym(s)||Ah; Ahb; Ahb-1; Ahhi; Ahrb; In|
|Gene Symbol and Name||Ahr, aryl-hydrocarbon receptor|
|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.|
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