Strain Name: |
C3H/HeJ |
|---|---|
Stock Number: |
000659 |
Availability: | Level 1 |
Price and Supply Information | |
General Terms and Conditions |
| Former Name |
C3H/HeJ-Pde6brd1 (Changed: 19-MAR-08
) |
| Strain Common Names | C3; C3H Heston; |
| Genes & Alleles | Gria4; Gria4spkw1; Pde6b; Pde6brd1; Tlr4; Tlr4Lps-d; In(6)1J; |
Product Information
Strain Details
Type Inbred Strain Additional information on Inbred Strains. Type JAX® GEMM® Strain - Spontaneous Mutation Additional information on JAX® GEMM® Strains. Mating System Sibling x Sibling (Female x Male) Species laboratory mouse H2 Haplotype k Generation F263 (03-JAN-08) Appearance
agouti
Related Genotype: A/AImportant Note
This strain does not carry mouse mammary tumor virus (MMTV). See JAX Notes, May 2000, #480. This strain is homozygous for retinal degeneration allele Pde6brd1, the defective lipopolysaccharide response allele Tlr4Lps-d, and for a chromosomal inversion on Chromosome 6.Strain Description
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. 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 18 months of age. 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. Visit the JAX ® Surgical Model for Alopecia Areata Web page for more information on this surgically induced model.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. See JAX Notes, Fall 2003, No. 491. The spontaneous mutation, spike wave discharge 1 (spkw1), is present in C3H/HeJ, but not C3HeB/FeJ. Mice homozygous for this mutation exhibit a modest incidence of absence seizures.
Strain Development
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.
Gene & Allele Details
| Allele Symbol | Gria4spkw1 | ||
|---|---|---|---|
| Allele Name | spike wave discharge 1 | ||
| Strain of Origin | C3H/HeJ | ||
| Gene Symbol and Name | Gria4, glutamate receptor, ionotropic, AMPA4 (alpha 4) | ||
| Chromosome | 9 | ||
| Gene Common Name(s) | GLUR4; GLUR4C; GLURD; GluR-D; Glur-4; Glur4; glutamate receptor 4; spike wave 1; spkw1; | ||
| 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 | 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 HeJ cerebella are reduced compared with controls. [MGI Ref ID J:135814] | ||
| Allele Symbol | In(6)1J | ||
| Allele Name | 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. [MGI Ref ID J:105810] [MGI Ref ID J:87486] | ||
| Allele Symbol | Pde6brd1 | ||
| Allele Name | retinal degeneration 1 | ||
| Common Name(s) | rd; rd-1; rd1; rodless retina; | ||
| Gene Symbol and Name | Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide | ||
| Chromosome | 5 | ||
| Gene Common Name(s) | CSNB3; PDEB; Pdeb; RP40; nmf137; phosphodiesterase, cGMP, rod receptor, beta polypeptide; r; rd; rd-1; rd1; rd10; retinal degeneration; retinal degeneration 1; retinal degeneration 10; | ||
| General Note |
Pde6brd1, retinal degeneration 1, recessive. Formerly r, rd, rd1. A mutation causing retinal degeneration described by Bruckner (J:25576) and by Tansley (J:15333) in various stocks was later found to be present in many inbred strains (J:114). Keeler (J:5007) thought it to be identical with the rodless retina mutation he had described in 1924 (J:24999); the identity has recently been proven by analyses of DNA from Keeler's original slides (J:15231). Homozygotes are fully viable and fertile.Eyes develop normally up to 7 to 10 days after birth. At this stage the outer segment of the rod cell has begun to form, and in wild type mice it elongates rapidly during the 10th to 15th days. In Pde6brd1/Pde6brd1 mice the nascent outer segments and the rod cells degenerate rapidly so that by 15 days there is only a thin layer of rod cells left, and they have disappeared completely by 35 days (J:5250, J:5708). The inner nuclear layer and the retinal ganglion cells appear normal butmay show slight quantitative reduction (J:5812, J:5292). Although the eyes of Pde6brd1 homozygotes are devoid of normal rods, the mice have some visual capacity (J:5980). About 3% of cones among the visual cells degenerate at a much slower rate than do rods, so that a few cones are still present at 18 months (J:5988). The surviving cones are postulated (J:25157) as the light receptors required for the persistence of circadian responses to dawn and dusk in Pde6brd1 homozygotes past the sstage when rods have disappeared (J:29236). In fusion chimeras between wild type and Pde6brd1 homozygous embryos, the Pde6brd1 mutant acts in the photoreceptor cells rather than in the pigment epithelium of the retina (J:5708). Action within photoreceptor cells is also implied by the long term survival of wild type rod cells transplanted into Pde6brd1 homozygote retinas (J:20769). At a stage before degeneration can be seen, a deficiency of cGMP-PDE, andan excess of cGMP, appears in rod photoreceptor cells (J:5332). The rate of retinal degeneration in mutants doubly homozygous for two retinal degeneration mutations (Pde6brd1 and RdsRd2) is intermediate between those of the two homozygotes (J:12044). The double homozygote shows an intermediate level of mRNAs for the ß subunit of cGMP-PDE and for several other phototransduction related proteins, suggesting an interaction between Pde6brd1 and RdsRd2 (J:2579). Genbank ID for mutant sequence: M75166 | ||
| 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. [MGI Ref ID J:11513] [MGI Ref ID J:4366] [MGI Ref ID J:51361] | ||
| Allele Symbol | Tlr4Lps-d | ||
| Allele Name | defective lipopolysaccharide response | ||
| Common Name(s) | TLR4-Mu; Tlr4-; Tlr4d; TlrLps-d; lpsd; | ||
| Strain of Origin | C3H/HeJ | ||
| Gene Symbol and Name | Tlr4, toll-like receptor 4 | ||
| Chromosome | 4 | ||
| Gene Common Name(s) | ARMD10; CD284; Lps; RAS-like, family 2, locus 8; Rasl2-8; TOLL; hToll; lipopolysaccharide response; | ||
| 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. The substitution of an A to C at nucleotide position 2342, results in an amino acid substitution that replaces proline with histidine at position 712. [MGI Ref ID J:51522] [MGI Ref ID J:53519] [MGI Ref ID J:57938] | ||
Colony Maintenance
| Diet Information | LabDiet® 5K52/5K67 |
|---|
Related Strains
C3H Strains
005972 C3H/HeJBirLtJ 001824 C3H/HeJSxJ 000635 C3H/HeOuJ 000474 C3H/HeSn 000661 C3H/HeSnJ 000658 C3HeB/FeJ 001908 C3HfB/BiJ View C3H Strains (7 strains)
002930 C.C3-Tlr4Lps-d/J 005973 C3Bir.129P2(B6)-Il10C3Bir/LtJ 004326 C3Bir.129P2(B6)-Il10tm1Cgn/Lt 003968 C3Bir.129P2(B6)-Il10tm1Cgn/LtJ 005972 C3H/HeJBirLtJ
004297 B6.CXB1-Pde6brd10/J 002802 C3.BLiA Pde6b+-Krd/J 001979 C3A.BLiA-Pde6b+.O20-Prph2Rd2/J 001912 C3A.BLiA-Pde6b+/J 003648 C3Sn.BLiA-Pde6b+/Dn 004766 C57BL/6J-Pde6brd1-2J/J 004828 FVB.129P2-Pde6b+ Tyrc-ch/AntJ 004808 STOCK Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
007227 B6.B10ScN-Tlr4lps-del/JthJ 003752 C57BL/10ScNJ
Phenotypic Data
Body Weight Information - JAX® Mice Strain C3H/HeJ (000659)Mouse Phenome Database
(This chart reflects the typical correlation between body weight and age for mice maintained in production colonies at The Jackson Laboratory.)
Mouse Phenome Database - body weight
Mouse Phenome Database - cardiovascular
Mouse Phenome Database - disease susceptibility
Mouse Phenome Database - ethanol effects
Mouse Phenome Database - food and water intake
Mouse Phenome Database - hematology
Mouse Phenome Database - lungs
Mouse Phenome Database / SNP Facility
Festing Inbred Strain Characteristics: C3H
NEW -- JAX® Physiological Data Summary
NEW -- JAX® Physiological Data Protocol
Additional Web Information
NEW -- JAX® Physiological Data Protocol
NEW -- JAX® Physiological Data Summary
A Surgically Induced Model of Alopecia Areata.
C3H strains free of exogenous MMTV
Genetic Quality Control Annual Report
JAX Notes, April 1988; 433. H-2 Haplotypes of Mice from Jackson Laboratory Production Colonies.
JAX Notes, Fall 2003; 491. Chromosomal Inversion Discovered in C3H/HeJ Mice.
JAX Notes, January 1988; 432. Arthritis Models in the Mouse.
JAX Notes, July 1987; 430. LPS Responsiveness of C3H Substrains.
JAX Notes, July 1987; 430. Mammary Tumor Incidence in C3H/HeJ and C3H/OuJ.
JAX Notes, Spring 1995; 461. Neoplastic and Hyperplastic Lesions in the C3H/HeJ Mouse Strain.
JAX Notes, Spring 2003; 489. Malocclusion in the Laboratory Mouse.
JAX Notes, Spring 2005; 497. Update of Chromosome 6 Inversion in JAX® Mice Strain C3H/HeJ.
JAX Notes, Summer 2003; 490. Hydrocephalus in Laboratory Mice.
JAX Notes, Summer 2005; 498. Toll-like Receptor JAX® Mice for Immunological Research.
JAX Notes, Winter 2006; 504. JAX® Mice: the Gold Standard Just Got Better.
JAX Notes, Winter 2006; 504. Reliable New Sperm Cryopreservation Service Developed at The Jackson Laboratory.
Animal Health Reports
Room Number AX10
Room Number AX3
Room Number AX4
Research Applications
This mouse can be used to support research in many areas including:
Pde6brd1 relatedCancer Research
Increased Tumor Incidence (Hepatomas)
Increased Tumor Incidence (Mammary Gland Tumors: late onset)
Cardiovascular Research
Diet-Induced Atherosclerosis (Relatively Resistant)
Immunology and Inflammation Research
Immunodeficiency (Tlr deficiency)
Neurobiology Research
Epilepsy
Research Tools
General Purpose
Sensorineural Research
Retinal Degeneration (Homozygous for Pde6brd1)
Tlr4Lps-d relatedMouse/Human Gene Homologs
retinitis pigmentosa, autosomal recessive
Sensorineural Research
Retinal Degeneration
Immunology and Inflammation Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers (Tlr deficiency)
Immunodeficiency (Tlr deficiency)
Inflammation (Tlr deficiency)
References
Selected Reference(s)
Additional ReferencesDragani TA; Manenti G; Gariboldi M; Degregorio L; Pierotti MA. 1995. Genetics of liver tumor susceptibility in mice. Toxicol Lett 82-3:613-619. [PubMed: 8597117] [MGI Ref ID J:31816]
Heston WE; Vlahakis G. 1971. Mammary tumors, plaques, and hyperplastic alveolar nodules in various combinations of mouse inbred strains and the different lines of the mammary tumor virus. Int J Cancer 7(1):141-8. [PubMed: 4322934] [MGI Ref ID J:24674]
Outzen HC; Corrow D; Shultz LD. 1985. Attenuation of exogenous murine mammary tumor virus virulence in the C3H/HeJ mouse substrain bearing the Lps mutation. J Natl Cancer Inst 75(5):917-23. [PubMed: 2997536] [MGI Ref ID J:24864]
Paigen B; Ishida BY; Verstuyft J; Winters RB; Albee D. 1990. Atherosclerosis susceptibility differences among progenitors of recombinant inbred strains of mice. Arteriosclerosis 10(2):316-23. [PubMed: 2317166] [MGI Ref ID J:22615]
Price and Supply Information
| Strain Name: | C3H/HeJ |
| Stock Number: | 000659 |
Price Details
IMPORTANT NOTE: Prices are based on shipping destination. The shipping destinations are:
- USA, Canada and Mexico
- International
*Pricing for Shipping Destination selected:
USA, Canada and Mexico
| Price(s) in US dollars ($) | Genotype(s) Provided | ||||
|---|---|---|---|---|---|
| 3 weeks | $17.50 | Female | |||
| 4 weeks | $17.50 | Female | |||
| 5 weeks | $17.50 | Female | |||
| 6 weeks | $19.40 | Female | |||
| 7 weeks | $21.30 | Female | |||
| 8 weeks | $23.20 | Female | |||
| 9 weeks | $23.60 | Female | |||
| 10 weeks | $27.30 | Female | |||
| 11 weeks | $27.30 | Female | |||
| 12 weeks | $27.30 | Female | |||
| 13 weeks | $29.20 | Female | |||
| 14 weeks | $31.10 | Female | |||
| 15 weeks | $33.00 | Female | |||
| 3 weeks | $15.65 | Male | |||
| 4 weeks | $15.65 | Male | |||
| 5 weeks | $15.65 | Male | |||
| 6 weeks | $17.55 | Male | |||
| 7 weeks | $19.45 | Male | |||
| 8 weeks | $21.35 | Male | |||
| 9 weeks | $22.30 | Male | |||
| 10 weeks | $26.00 | Male | |||
| 11 weeks | $26.00 | Male | |||
| 12 weeks | $26.00 | Male | |||
| 13 weeks | $27.90 | Male | |||
| 14 weeks | $29.80 | Male | |||
| 15 weeks | $31.70 | Male | |||
Supply Details
| Standard Supply | JAX Ready Strain® (Level 1). Most popular strains. Readily available in any quantity you need. |
|---|---|
| Supply Notes |
Histology and Tissue Collection Services are available for all JAX® Mice strains. For more information, please contact Customer Service at orderquest@jax.org or 1-800-422-6423. Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available. Strains that must be genotyped are not available until five to seven weeks of age. Timed pregnant females are available from the Bar Harbor facility. Genomic DNA is available for this strain from the Mouse DNA Resource. |
| Licensing | See General Terms and Conditions below |
General Terms and Conditions
View JAX® Mice & Services Conditions of Use.
The Jackson Laboratory's Genotype Promise
The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.Ordering and Purchasing Information
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