C57BR/cdJ mice show variable incidence of spinal cord epidermoid cysts, primarily in the leptomeninges adjacent to the posterior horn and lateral/anterior columns. Mice of this strain show several behavioral differences from many other inbred strains.
Due to demand, this colony is being expanded. An estimated distribution date is provided above.
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This strain is homozygous for Cdh23ahl, the age related hearing loss 1 mutation, which on this background results in progressive hearing loss.
Due to demand, this colony is being expanded. An estimated distribution date is provided above.
C57BR/cdJ mice develop early-onset hearing loss that is moderate at seven weeks of age, is severe by 20 weeks and progresses with increasing age (Henry 1982; Zheng et al. 1999). The loss is greatest in the higher frequency range; at seven weeks, Henry reported 50% of the mice showed no 64 kHz auditory brainstem response (ABR), and by 100 days both the 2 kHz and 32 kHz responses were absent. Both labs found this strain to be least vulnerable to loss of the16 kHz response, which persisted through 200 days but was lost before 300 days of age (Henry 1982). C57BR/cdJ did not exhibit aberrant ABR wave patterns, suggesting that the hearing loss results from defects of the peripheral, rather than central auditory system (Zheng et al. 1999). F1 hybrid progeny from matings with the good-hearing strain CAST/Ei exhibited good hearing even at advanced ages, indicating that the allele(s) responsible for hearing loss in C57BR/cdJ are recessive. An allelism test between C57BR/cdJ and NOD.NON-H2nb1 showed the mutations responsible for hearing loss in these two strains not to be allelic; NOD.NON-H2nb1 shares the deafness allele(s) of A/J, ALR/LtJ and DBA/2J (Zheng et al. 1999).
C57BR/cdJ mice showed variable incidence of spinal cord epidermoid cysts, primarily in the leptomeninges adjacent to the posterior horn and lateral/anterior columns. The cysts comprised "a whorled mass of keratinized cells surrounded by polygonal epithelial cells," some of which contained keratohyaline granules. No basal cells were present. (Stroop 1884).
EEG studies demonstrated that although C57BR/cd mice spend less time sleeping, a greater proportion of their sleep time is spent in paradoxical sleep (PS)(equivalent to human rapid eye movement, or REM sleep) than is true of mice of six other inbred strains tested (Pagel et al. 1973). Whereas C57BL/6 mice learn slowly, gradually improving their performance at a rate dependent upon the number of training trials, C57BR/cd mice fail to improve during the initial training, but show improvement after a delay of at least eight to 10 hours; overall, C57BR/cd mice are fast learners. PS deprivation has no effect on either discriminatory or active avoidance learning in C57BL/6, BALB/c or SEC mice. In contrast, PS deprivation for 24 hours impairs learning of discriminatory tasks by C57BR/cd mice, and six hours' PS deprivation immediately following the initial training abolishes their time-dependent improvement in avoidance learning. Continuous PS deprivation causes C57BR/cd mice to learn at the same rate as C57BL/6 mice. Interestingly, although BALB/c mice show a time-delayed improvement in learning acquisition for an appetitive task similar to that of C57BR/cd mice for avoidance learning, neither C57BR/cd nor C57BL/6 exhibit show such time-dependent improvement in appetitive learning (Kitahama et al. 1981 and references cited therein).
Created by C.C. Little from a cross that gave rise to C57BL, C57BR/a, and C57L. Black and brown lines were separated in the first generation. Subline cd was established in generation 13 from a cross of two brown lines, one of which had previously given rise to C57BR/a. Obtained by The Jackson Laboratory from W. E. Heston at F66.
|Allele Name||b-1 variant|
|Allele Type||Not Applicable (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; 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.|
|Allele Name||MCF sensitive|
|Gene Symbol and Name||Rmcf, resistance to MCF virus|
|Strain of Origin||multiple strains|
|General Note|| |
This locus controls resistance and susceptibility of cells in tissue culture to infection by mink cell focus-forming murine leukemia viruses. The allele Rmcfr determines resistance and occurs in strains DBA/1, DBA/2, and CBA/Ca; the allele Rmcfs determines susceptibility and occurs in strains AKR/J, C57BL/6, BALB/c, CBA/J, NFS, NZB, 129/J, and many others. Heterozygotes are as resistant as the resistant parent or nearly so. Rmcf is different from and independent of Fv1, a locus that controls susceptibility to infection by ecotropic viruses. Rmcf is located on Chr 5 close to Hm near the centromeric end (J:7108). Rmcfr protects (AKR x CBA/Ca)F1 and (AKR x DBA/2)F1 hybrids from development of spontaneous thymic lymphomas and reduces the incidence of MCF-induced thymic lymphomas (J:7175). It also reduces susceptibility of cells of Sxvs/Sxvr mice to exogenous xenotropic viruses (J:7951). In addition, in strains susceptible to Friend virus-induced erythroleukemia, a condition thought to be due to the replication of MCF virus, Rmcfr increases resistance to the virus-induced erythroleukemia. It may cause resistance by coding for or regulating the production of an MCF-related envelope glycoprotein that blocks the receptor for MCF viruses (J:8074). This conclusion is reinforced by the findings of Buller et al. (J:8497), who showed that the Rmcfr allele contains an endogenous MCF gp70 env gene and that the Rmcfs allele, at least in some strains (C57BL/6, CBA/J, and A/WySn), contains a xenotropic gp70 env gene. Presumably the MCF gp70 inhibits exogenous MCF infection in vitro by a mechanism of viral interference.
|Molecular Note||This locus controls resistance of cells to infection by mink cell focus-forming murine leukemia viruses. The recessive s (susceptible) allele is found in AKR/J, C57BL/6, BALB/c, CBA/J, NFS, NZB and 129/J.|
This inbred strain is maintained by sibling mating.
When using the C57BR/cdJ mouse strain in a publication, please include JAX stock #000667 in your Materials and Methods section.
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided,
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