CXB5/ByJ

Stock number: 000355
Research areas: Cell Biology Research, Developmental Biology Research, Mouse/Human Gene Homologs, Neurobiology Research, Reproductive Biology Research, Research Tools, Sensorineural Research

Description

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.

Detailed description

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 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

Gene Network.

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).

Development

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

Symbol: Hld
Name: hippocampal lamination defect
MGI accession ID: MGI:2447987
Generation method: Spontaneous
Marker symbol: Hld
Marker name: hippocampal lamination defect
Chromosome: UN
Strain of origin: BALB/cJ

Allele

Symbol: Crb1^rd8
Name: retinal degeneration 8
MGI accession ID: MGI:2676366
Generation method: Spontaneous
Marker symbol: Crb1
Marker name: crumbs family member 1, photoreceptor morphogenesis associated
Chromosome: 1
Strain of origin: C57BL/6By or C57BL/6N
Molecular note: The mutation in the rd8 mouse has been identified as a single base deletion of a C (G on forward strand) at coding nucleotide 3481 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

Symbol: Ahr^b-2
Name: b-2 variant
MGI accession ID: MGI:2667355
Generation method: Not Applicable
Marker symbol: Ahr
Marker name: aryl-hydrocarbon receptor
Chromosome: 12
Strain of origin: BALB/cBy
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).
General note: C57BL/6 carries the responsive Ahr^b allele; DBA/2 carries nonresponsive Ahr^d. Heterozygotes (Ahr^b/Ahr^d) 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 Ahr^b-1; Ahr^b-2 is carried by BALB/cBy, A, and C3H; and Ahr^b-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 Ahr^b-1 and Ahr^d have been determined (J:17460).

Strain of origin - this allele was found in BALB/cByJ, A/J, C3H/HeJ, CBA strains

Allele

Symbol: Fgfr2^svs
Name: seminal vesicle shape
MGI accession ID: MGI:1856633
Generation method: Spontaneous
Marker symbol: Fgfr2
Marker name: fibroblast growth factor receptor 2
Chromosome: 7
Strain of origin: CXB5/By
Molecular note: An insertion of a 491-bp mouse leukemia virus long terminal repeat (MLV-LTR) sequence into intron 10 results in aberrant alternative splicing of the transcript with exclusion from most mature mutant mRNA species of exon 8IIIb, which encodes the domain required for specific binding to FGF ligands in developing prostate and seminal vesicle mesenchyme.
General note: This recessive autosomal mutation apparently occurred early in the inbreeding of the Essex CXB recombinant inbred lines, as the abnormality was not present in either of the parental strains, C57BL/6ByEss or BALB/cByEss, but is present in both CXBI/ByJax and CXBI/ByLac J:9441.