C3H/HeJ mice, commonly called C3H, are used as a general purpose strain in a wide variety of research areas including cancer, infectious disease, sensorineural, and cardiovascular biology research. A spontaneous mutation in Tlr4 occurred in C3H/HeJ at the lipopolysaccharide response locus (mutation in toll-like receptor 4 gene, Tlr4Lps-d) making C3H/HeJ mice more resistant to endotoxin. C3H/HeJ mice are highly susceptible to infection by Gram-negative bacteria such as Salmonella enterica. The C3H substrains at The Jackson Laboratory are homozygous for the retinal degeneration 1 mutation (Pde6brd1), causing blindness by weaning age.Read More +
This strain does not carry mouse mammary tumor virus (MMTV). This strain is homozygous for retinal degeneration allele Pde6brd1, the defective lipopolysaccharide response allele Tlr4Lps-d, and for a chromosomal inversion on Chromosome 6. A sighted alternative is Stock No. 003648, C3Sn.BLiA-Pde6b+/DnJ.
C3H/HeJ mice are used as a general purpose strain in a wide variety of research areas including cancer, immunology and inflammation, sensorineural, and cardiovascular biology. C3H/HeJ mice and all other Jackson substrains are homozygous for the retinal degeneration 1 mutation (Pde6brd1), which causes blindness by weaning age, but lack the nob5 allele of Gpr179 (Chang, 2015). White belly spots, ranging in phenotype from a few white hairs to a defined spot are common in C3H/HeJ mice. There is also a high incidence of hepatomas in C3H mice (reportedly 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females). Despite the lack of exogenous mouse mammary tumor virus (MMTV), virgin and breeding females may still develop some mammary tumors later in life. C3H/HeJ mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, Stock No. 000667, and SM/J, Stock No. 000687). C3H/HeJ mice spontaneously develop alopecia areata (AA) at a reported incidence of approximately 0.25% by 5 months of age. In older mice (12-18 months old), incidences as high as approximately 20% are reported. Females as young as 3-5 months can develop AA, but onset typically is delayed until after 6 months in males. Alopecia areata can be surgically-induced by grafting a small piece of skin from an older, donor animal with AA onto a younger, isogenic C3H/HeJ recipient.
A spontaneous mutation occurred in C3H/HeJ at the lipopolysaccharide response locus (later identified as a mutation in the toll-like receptor 4 gene, Tlr4Lps-d) making C3H/HeJ mice endotoxin resistant. C3H/HeJ (Tlr4Lps-d) mice are highly susceptible to infection by Gram-negative bacteria such as Salmonella enterica. Mice infected with Salmonella exhibit delayed chemokine production, impaired nitric oxide generation and attenuated cellular immune responses. Mortality in infected mice appears to result from enhanced bacterial growth within the liver Kupffer cell network (Vazquez-Torres et al., 2004).The C3H/HeJ substrain is homozygous for an inversion on Chromosome 6 (symbol: In(6)1J). The inversion covers 20% of Chromosome 6 between D6Mit124 (~30.3 cM) and D6Mit150 (~51.0 cM), but results in no reported phenotype. Results from screening other C3H substrains and cryopreserved stock from C3H/HeJ suggest that the mutation arose after 1952. The spontaneous mutation, spike wave discharge 1 (Gria4spkw1), is present in C3H/HeJ, but not C3HeB/FeJ. Mice homozygous for this mutation exhibit a modest incidence of absence seizures. This strain is also homozygous for a hypomorphic allele in Pcnx2, which is caused by an IAP insertion and which dampens the severity of the absence seizure phenotype caused by Gria4spkw1 (Frankel et al., 2014).
The C3H parent strain was developed by LC Strong in 1920 from a cross of a Bagg albino female with a DBA male followed by selection for high incidence of mammary tumors. This high incidence resulted from exogenous mouse mammary tumor virus (MMTV) transmitted through the mother's milk. The Jackson Laboratory maintains four C3H substrains, C3H/HeJ (Stock No. 000659), C3H/HeOuJ (Stock No. 000635), C3HeB/FeJ (Stock No. 000658) and C3H/HeSnJ (Stock No. 000661) that are now free of exogenous MMTV. C3H/HeJ and C3H/HeOuJ mice previously carried MMTV but were rederived in 1999 during planned efforts to increase the overall health status of the mice and the virus was not reintroduced. C3H/HeJ and C3H/HeOuJ substrains were separated in 1952 and are genetically very similar. However, a spontaneous mutation occurred in C3H/HeJ sometime between 1960 and 1968 at lipopolysaccharide response locus (mutation in toll-like receptor 4 gene, Tlr4lps) making C3H/HeJ mice endotoxin resistant while the other three C3H strains are endotoxin sensitive.
|Allele Name||b-2 variant|
|Allele Type||Not Applicable|
|Allele Synonym(s)||Ahb-2; Ahh|
|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||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).|
|Allele Name||a variant|
|Allele Type||Spontaneous (Not Applicable)|
|Allele Synonym(s)||CD5.1; Ly-1.1|
|Gene Symbol and Name||Cd5, CD5 antigen|
|Gene Synonym(s)||LEU1; Ly-1; Ly-1; Ly-12; Ly-12; Ly-A; Lyt-1; Lyt-1; T-lymphocyte antigen 1; T1; lymphocyte antigen 1; lymphocyte antigen 12|
|Strain of Origin||multiple strains|
|Molecular Note||Sequence analysis of C3H/HeJ showed that this polymorphic variant has point mutations relative to the b variant that result in valine instead of isoleucine at amino acid 9, leucine instead of glutamine at amino acid 52, and isoleucine instead of phenylalanine at amino acid 71, all within the amino terminal scavenger receptor cysteine-rich D1 domain, in addition to 7 silent point mutations. This allele is found in many inbred strains including CBA/J, C3H and DBA substrains.|
|Allele Name||spike wave discharge 1|
|Gene Symbol and Name||Gria4, glutamate receptor, ionotropic, AMPA4 (alpha 4)|
|Gene Synonym(s)||GLUR4; GLUR4C; GLURD; GluA4; GluR-D; GluR4; Glur-4; Glur-4; Glur4; Glur4; Gluralpha4; NEDSGA; glutamate receptor 4; spike wave 1; spkw1; spkw1|
|Strain of Origin||C3H/HeJ|
|General Note||This allele interacts with spkw2. Animals with the highest incidence of spike wave discharges are homozygous for C3H/HeJ-derived alleles at spkw1 and heterozygous for C57BL/6J and C3H/HeJ alleles at spkw2.|
|Molecular Note||This mutation was originally identified as a QTL allele conferring increased incidence of spike wave discharges in the brains of C3H/HeJ mice as compared to C57BL/6J. Genomic PCR and sequencing showed a full-length intracisternal A-particle (IAP) proviral insertion in the last intron of Gria4 in C3H/HeJ mice. qRT-PCR showed a 10-fold difference in C3H/HeJ and C3HeB/FeJ substrains in transcripts detected between exons flanking the IAP-containing intron, and a neglible difference between upstream exon transcript levels in these substrains. Gria4 protein levels in C3H/HeJ cerebella are reduced compared with controls.|
|Allele Name||inversion, Chr 6, Jackson 1|
|Gene Symbol and Name||In(6)1J, inversion, Chr 6, Jackson 1|
|Strain of Origin||C3H/HeJ|
|General Note||C3H/HeJ and C3H/HeJBir carry this inversion; C3H/HeSnJ and C3HeB/FeJ do not. Examination of recombination distances in Recombinant Inbred (RI) strain sets developed using C3H/HeJ as a progenitor suggest none of these harbor the inversion. Mouse strains carrying spontaneous mutations that arose on the C3H/HeJ background after 1965-1970 could carry the inversion and are expected to if the mutation arose after the early 1970s.|
|Molecular Note||The In(6)1J inversion covers approximately 20% of Chr 6 in C3H/HeJ mice. Therefore, linkage crosses using C3H/HeJ will show no recombination in this region of Chr 6. Genetic analyses of congenic construction crosses suggested that the suppressed region lies between D6Mit124 (cytological band 6C3) and D6Mit150 (cytological band 6F1). FISH analyses using flanking BACs detected a paracentric chromosomal region between ~73 Mb and ~116 Mb.|
|Allele Type||Spontaneous (Hypomorph)|
|Gene Symbol and Name||Pcnx2, pecanex homolog 2|
|Gene Synonym(s)||AU067631; E330039K12Rik; E330039K12Rik; PCNXL2; Pcnxl2; Pcnxl2; RGD1305883; RIKEN cDNA E330039K12 gene; expressed sequence AU067631; pecanex-like 2 (Drosophila)|
|Strain of Origin||C3H/HeJ|
|Molecular Note||This IAP insertion in intron 19 causes diminished expression of this gene by RT-PCR in C3H/HeJ and is not found in C3HeB/FeJ, C3H/HeOuJ, or C3H/HeSnJ.|
|Allele Name||retinal degeneration 1|
|Allele Synonym(s)||Pdebrd1; rd; rd-1; rd1; rodless retina|
|Gene Symbol and Name||Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide|
|Gene Synonym(s)||CSNB3; CSNBAD2; GMP-PDEbeta; PDEB; Pdeb; Pdeb; RP40; nmf137; phosphodiesterase, cGMP, rod receptor, beta polypeptide; r; r; rd; rd; rd-1; rd1; rd1; rd10; rd10; retinal degeneration; retinal degeneration 1; retinal degeneration 10|
|Strain of Origin||various|
|General Note||The following inbred strains are known to be homozygous for Pde6b |
|Molecular Note||Two mutations have been identified in rd1 mice. A murine leukimia virus (Xmv-28) insertion in reverse orientation in intron 1 is found in all mouse strains with the rd1 phenotype. Further, a nonsense mutation (C to A transversion) in codon 347 that results in a truncation eliminating more than half of the predicted encoded protein, including the catalytic domain has also been identified in all rd1 strains of mice. A specific degradation of mutant transcript during or after pre-mRNA splicing is suggested.|
|Allele Name||defective lipopolysaccharide response|
|Allele Synonym(s)||TLR4-M; TLR4-Mu; TLR4lps-def; TLR4d; Tlr4-; Tlr4d; TlrLps-d; lpsd; mutant TLR4|
|Gene Symbol and Name||Tlr4, toll-like receptor 4|
|Gene Synonym(s)||ARMD10; CD284; Lps; Lps; RAS-like, family 2, locus 8; Rasl2-8; Rasl2-8; TLR-4; TOLL; lipopolysaccharide response; lipopolysaccharide response|
|Strain of Origin||C3H/HeJ|
|General Note||C3H/HeJ mice carry this allele. Various combinations of Lps-associated traits have been followed in crosses between C3H/HeJ and other C3H substrains, and the traits have in all cases segregated together (J:30692, J:5557, J:5593, J:5938). Some of the traits show dominance of the Tlr4lps-n allele; others, including Tlr4Lps-d, show codominance. |
Genbank ID for this allele: AF095353
|Molecular Note||This allele corresponds to a mutation in the third exon of the gene. A C to A substitution at nucleotide position 2342 results in an amino acid substitution that replaces proline with histidine at position 712.|
When using the C3H mouse strain in a publication, please include JAX stock #000659 in your Materials and Methods section.
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