The CXB set of RI strains is used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in thyroid function (Graves' disease) and pulmonary inflammation as well as behavioral phenotypes including avoidance, exploration and locomotor activity. The CXB set is derived from the BALBc/ByJ (Stock No. 001026) and C57BL/6ByJ (Stock No. 001139) progenitor strains.Read More +
The CXB set of RI strains is used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in thyroid function (Graves' disease), contact dermatitis, and pulmonary inflammation as well as behavioral phenotypes including avoidance, exploration and locomotor activity.
The strain distribution pattern (SDP) for the CXB RI strains is available through the Mouse Genome Informatics
Contributed Data Sets and Gene Network.
Additional tools and information are presented through the Mouse Phenome Database
Specialized Strain Panel Query Form, and
The CXB set is so small that markers on different chromosomes occasionally have almost precisely the same SDP. This produces high non-syntenic association and false linkage between variance in phenotypes and genotypes. Please examine the correlation coefficients of markers close to interest loci with ALL other markers to evaluate the risk of non-syntenic association.
Like BALB/cByJ, this recombinant inbred carries the mutation hippocampal lamination defect or Hld, an allele responsible for abnormal neuronal migration to the pyramidal cell layer (Nowakowski RS, et al, Jnl Neurogen, 1984).
The original 11 CXB recombinant inbred (RI) lines were generated at the National Institutes of Health by Dr. Donald Bailey (labcode By) starting in 1959. After moving to The Jackson Laboratory in 1967, an additional set of 6 strains was created with the help of Jo Hilgers (Labcode Hi). The CXB set is derived from the BALBc/ByJ (Stock No. 001026) and C57BL/6ByJ (Stock No. 001139) progenitor strains. CXB1 through CXB7 originally were designated using letters. Several of the original strains are extinct. The Jackson Laboratory currently distributes 7 of the original By strains and 6 of the Hi strains.
|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.|