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 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.
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
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-2 variant|
|Allele Type||Not Applicable|
|Allele Synonym(s)||Ahb-2; Ahh|
|Gene Symbol and Name||Ahr, aryl-hydrocarbon receptor|
|Strain of Origin||BALB/cBy|
|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 BALB/cByJ, A/J, C3H/HeJ, CBA strains
|Molecular Note||This allele encodes a high affinity, heat labile, 104 kDa receptor containing 848 amino acids. Sequencing studies of cDNA from C57BL/6J congenic mice homozygous for this allele identified nucleotide substitutions in the ORF that would cause 5 amino acid differences between the C57BL/6J and BALB/cBy peptides, and 2 amino acid differences between the BALB/cBy and DBA/2J peptides. A T to C transition in exon 11 replaces the opal termination codon in the C57BL/6J allele with an arginine codon in the BALB/cBy allele. This change would extend translation of the BALB/cBy mRNA by 43 amino acids, accounting for the larger size of the peptide produced by this allele (104 kDa, vs 95 kDa for the C57BL/6J allele).|
When using the CXB4/ByJ mouse strain in a publication, please cite the originating article(s) and include JAX stock #000354 in your Materials and Methods section.