This C57BL/6ByJ substrain, closely related to C57BL/6NJ, does not have the nicotinamide nucleotide transhydrogenase (Nnt) gene deletion found in C57BL/6J, and does have the Crb1rd8 mutation that is absent from C57BL/6J.Read More +
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 is C; 11-004367508-M is A; 13-041017317-M is C; 15-057561875-M is G; 19-049914266-M is T. C57BL/6J types as follows: 08-015199792-M is T; 11-004367508-M is G; 13-041017317-M is T; 15-057561875-M is A; 19-049914266-M is G (Petkov and Wiles, 2005.)
In 1951 C57BL/6J, then at generation F32, was sent from The Jackson Laboratory to The National Institute of Health where they were maintained via sibling inbreeding for decades. Dr. Donald Bailey oversaw the breeding stocks in the NIH in the late 1950?s. When he took a position at The University of California, San Francisco, in 1961 he took with him breeder pairs of C57BL/6JN from which he maintained his own subline. When he returned to The Jackson Laboratory in 1967 he brought this line with him and when he transferred breeder pairs to the production facility at The Jackson Laboratory this inbred strain received the subline designation C57BL/6ByJ.
|Allele Name||retinal degeneration 8|
|Allele Synonym(s)||Crb1rd8; retinal degeneration 8|
|Gene Symbol and Name||Crb1, crumbs family member 1, photoreceptor morphogenesis associated|
|Gene Synonym(s)||7530426H14Rik; A930008G09Rik; RIKEN cDNA 7530426H14 gene; RIKEN cDNA A930008G09 gene; LCA8; 7530426H14Rik; RP12; A930008G09Rik|
|Strain of Origin||C57BL/6By or C57BL/6N|
|Molecular Note||The mutation in the rd8 mouse has been identified as a single base deletion at nt3481 in the gene. This deletion causes a frame shift and a premature stop codon that truncates the transmembrane and cytoplasmic domain of the protein after amino acid 1207. This mutation has been found to be present in all sublines of C57BL/6N and in C57BL/6ByJ, but not in any C57BL/6J subline. It occurred sometime between transfer of mice from JAX to NIH, in 1951, and from NIH to Donald Bailey, in 1961.|
|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.|
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