FVB/NJ are a widely used multipurpose inbred strain. Due to the prominent pronuclei in their fertilized eggs and the large litter size, FVB/NJ are commonly used for transgenic injection. FVB/NJ mice are homozygous for the retinal degeneration 1 allele of Pde6brd1, resulting in blindness by wean age.Read More +
This strain is homozygous for the retinal degeneration allele Pde6brd1.
FVB/NJ was inbred for the Fv1b allele which confers sensitivity to the Friend leukemia virus B strain. Due to the prominent pronuclei in their fertilized eggs and the large litter size, FVB/NJ mice are commonly used for transgenic injection. Compared to many other inbred strains, FVB/NJ is highly susceptible to asthma-like airway responsiveness with significant generation of antigen-specific IgE. Despite having the H2q MHC haplotype, FVB/NJ are resistant to collagen-induced arthritis. This resistance stems from coding polymorphisms in Tcra-V11.1 and a genomic deletion of some Tcrb-V genes that includes Tcrb-V8.2. FVB/NJ have higher than average activity, anxiety, and basal body temperature, low stress-induced hyperthermia, and are homozygous for the Pde6brd1 allele, which results in early onset retinal degeneration. Although FVB/N typically do not develop spontaneous tumors, they are highly susceptible to chemically induced squamous cell carcinomas with a high rate of malignant conversion from papilloma to carcinoma. For more information, please refer to Michael Festing's Index of Inbred Strain Characteristics.
In 1966, outbred Swiss mice at the National Institutes of Health were selectively bred for either resistance or sensitivity to histamine challenge post pertussis vaccination. At the eighth generation of inbreeding (in the early 1970s), the sensitive line, HSFS/N, was found to carry the Fv1b allele which confers sensitivity to the Friend leukemia virus B strain. The FVB/N strain resulted from inbreeding this line for the Fv1b allele. In 1988 FVB/N mice were imported from NIH to Dr. Taketo at The Jackson Laboratory and in 1991 these were re-derived at F50 into the foundation stocks facility at The Jackson Laboratory. In December 2002 this strain reached F87.
|Allele Synonym(s)||Bfsp2Dundee; Dundee|
|Gene Symbol and Name||Bfsp2, beaded filament structural protein 2, phakinin|
|Gene Synonym(s)||CP47; CP49; CTRCT12; LIFL-L; expressed sequence AI448593; PHAKOSIN; AI448593|
|Strain of Origin||129X1/SvJ|
|Molecular Note||A deletion of ~6 kb within intron B was identified in the 129X1/SvJ background. The deleted region included 24 bp of the exon 2 splice acceptor site. RT-PCR analysis identified transcript in which exon 2 is skipped and exon 1 splices directly to exon 3. The aberrant splicing generates a frameshift and ultimately a premature stop codon at position 2 of exon 3. Neither normal protein nor truncated fragments were detected by Western blot analysis. This mutation has been detected in 129S1/SvImJ, 129S2/SvPas, 129S4/SvJae, FVB/N, NZB/BlNJ, and NZW/LacJ backgrounds but not in C3H or C57BL/6J backgrounds.|
|Allele Type||Spontaneous (Not Specified)|
|Allele Synonym(s)||deletion; Gpr84del|
|Gene Symbol and Name||Gpr84, G protein-coupled receptor 84|
|Gene Synonym(s)||GPCR4; EX33|
|Strain of Origin||multiple strains|
|Molecular Note||This spontaneously arising frameshift deletion is located in exon 2 at position 103308576 bp (NCBI Build 37) and results in a premature stop codon. The mutation is predicted to result in a truncated protein lacking the transmembrane domains 4-7. The inbred strains BDP/J, DBA/1J, DBA/2J, I/LnJ, FVB/NJ, LG/J, MRL/MpJ, NODShi/LtJ, NOR/LtJ, P/J, PL/J, SKHIN/Sprd, SJL/J, SM/J are homozygous for the deletion. The allele is segregating in the outbred stocks ICR and CD-1.|
|Allele Synonym(s)||deficient; Hc0|
|Gene Symbol and Name||Hc, hemolytic complement|
|Gene Synonym(s)||He; CPAMD4; ECLZB; C5b; He; C5; C5a; C5D; C5; Hfib2; hepatic fibrogenesis 2; Hfib2|
|Strain of Origin||multiple strains|
|General Note|| |
This is an allele characteristic of various inbred mouse strains including the following: A/HeJ, A/J, AKR/J, DBA/2J, NZB/B1NJ, SWR/J, B10.D2/oSnJ
Hc was identified as a candidate gene for Abhr2 in a microarray analysis of lung mRNA from A/J, C3H/HeJ, and (A/J x C3H/HeJ)F1 x A/J backcross animals. Hc genotype shows statistically significant correlation to allergen-induced bronchial hyperresponsive phenotype. The A/J allele contains a 2 bp deletion resulting in deficient Hc mRNA and protein production and is associated with susceptibility to allergen-induced bronchial hyperresponsiveness. (J:108211)
|Molecular Note||A 2 base "TA" deletion at positions 62 and 63 of an 83 base pair exon near the 5' end of the gene is found in the following mouse strains: A/HeJ, A/J, AKR/J, DBA/2J, I/LnJ, KK/HlJ, MOLF/EiJ, NZB/B1NJ, RF/J, ST/bJ SWR/J, B10.D2/oSnJ. The consequence of this deletion is the creation of a stop codon starting four bases after the deletion. A truncated product of 216 amino acids is predicted as a result although contradictory reports exist that a larger pro-C5 protein may be synthesized. Nevertheless, macrophages from mouse strains carrying this allele do not secrete complement 5.|
|Allele Synonym(s)||deletion; Disc1del|
|Gene Symbol and Name||Disc1, disrupted in schizophrenia 1|
|Gene Synonym(s)||SCZD9; C1orf136|
|Strain of Origin||various|
|General Note||This deletion appears in multiple strains of the 129 superfamily, 101/RI, BTBR T+ tf/J, LP/J, FVB/NJ, SJL/J, SWR/J and DDY/JclSidSeyFrkJ (J:111837, J:195189).|
|Molecular Note||A 25 bp deletion of the locus causes a frame shift in the reading frame, resulting in 13 novel amino acids and a premature stop codon at exon 7.|
|Allele Name||myxovirus susceptibility 1|
|Allele Synonym(s)||Mx1s1; myxovirus susceptibility 1|
|Gene Symbol and Name||Mx1, MX dynamin-like GTPase 1|
|Gene Synonym(s)||Mx; Mx-1; Mx; Mx-1; AI893580; myxovirus (influenza) resistance 1 polypeptide; expressed sequence AI893580; IFI-78K; MxA; MX; IFI78; MXB|
|Strain of Origin||multiple strains|
|General Note|| |
The Mx genes determine resistance to the lethal effects of various myxoviruses including neurotropic avian influenza A virus injected intracerebrally, pneumotropic strains injected intranasally, and a hepatotropic strain injected intraperitoneally (J:5645, J:13136). Resistance is not dependent on presence of the thymus and is not abolished by immunosuppression or by inhibitors of macrophage function (J:5735, J:5478, J:5645). Resistance is specific for the orthomyxoviruses (J:6265). It is dependent on the presence of interferon-alpha and -beta but not -gamma (J:7365).
The resistance allele at the Mx1 locus, under induction by alpha/beta interferon, produces the 75 kDa protein MX-1, which confers resistance to the influenza virus, in the nuclei of cells carrying the allele. Susceptibility alleles do not produce the protein (J:8273). The protein is located in the nucleus (J:7703) and produces its antiviral effect by preventing synthesis of viral mRNA in the nucleus (J:7992). Nuclear localization is necessary for anti-influenza virus activity (J:1417), but mutations induced in Mx1 showed that nuclear position was not sufficient for the effect; mutations in several domains can cause its loss (J:11840). The MX-1 protein is a GTPase containing a GTP binding domain (J:1417) and this binding core is also necessary (J:21243).
Resistance is expressed by macrophages and other cells in vitro (J:6649, J:5940) but could not be transferred to susceptible animals by transfer of macrophages from resistant mice (J:6149).
Resistance to infection with two tick-borne viruses, Thogoto virus (J:8273) and Dhori virus (J:27760), is also conferred by Mx1r.
The Mx1r allele occurs only in strains A2G, SL/NiA, and T9, the latter being a strain derived from an influenza-resistant wild stock, and CAST/Ei, derived from Mus musculus castaneus. Most inbred strains, including C57BL/6J, C3H/HeJ, and BALB/cJ, carry an influenza susceptible Mx1s1 allele which produces mRNA lacking exons 9, 10, and 11 of the Mx1r allele. This large deletion apparently renders the protein incapable of providing resistance to influenza. The CBA/J, CE/J, I/LnJ, and PERA/Ei strains, also susceptible to the virus, have another form of the Mx1s2 allele in which there is a nonsense mutation (J:9452).
Interferon is induced by viral infection and in turn induces the Mx protein (J:7703). Although some interferon-induced genes respond directly to virus invasion as well as indirectly through induction by virus-induced interferon, this primary response is very weak for the MX-1 protein in response to either influenza or Newcastle disease viruses (J:1892).
|Molecular Note||Many inbred mouse strains have an exon 9 to 11 deletion, resulting in a null allele and susceptibility to myxoviruses, including: A/J, ABP/Le, AKR/J, AU/SsJ, BALB/cJ, BDP/J, BUB/BnJ, C3H/HeJ, C57BL/6J, C57BL/10J, C57BL/KsJ, C57L/J, C58/J, DA/HuSn, DBA/2J, FSB/GnEi, FVB/NJ, LIS/A, LP/J, MA/MyJ, MAS/A, NZB/BINJ, P/J, PL/J, RIIIS/J, RF/J, SEA/GnJ, SEC1/ReJ, SJL/J, ST/bJ, TS1/A, TW1/A. YBR/Ei, 020/A, 129/J, SF/CamEi and SK/CamEi.|
|Allele Name||retinal degeneration 1|
|Allele Synonym(s)||retinal degeneration 1; Pde6brd1|
|Gene Symbol and Name||Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide|
|Gene Synonym(s)||rd; rd1; Pdeb; r; rd; rd10; nmf137; r; retinal degeneration; retinal degeneration 1; retinal degeneration 10; CSNB3; CSNBAD2; rd1; rd-1; rd10; PDEB; RP40; phosphodiesterase, cGMP, rod receptor, beta polypeptide; Pdeb; GMP-PDEbeta|
|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||mutation 1|
|Allele Synonym(s)||mutation 1; mt-Atp8m1|
|Gene Symbol and Name||mt-Atp8, mitochondrially encoded ATP synthase 8|
|Gene Synonym(s)||URFA6L; ATPase8; MTATP8|
|Strain of Origin||FVB/NJ|
|Molecular Note||A G to T transversion is located at nucleotide 7778 resulting in an aspartic acid to tyrosine substitution in the fifth amino acid of the conserved N-terminus of the protein. This substitution has been reported in the FVB/NJ strain.|
|Marker Synonym(s)||Rv-1; Fv-1; Fv-1; Rv-1; Rv1; Rv1; Rauscher leukemia virus susceptibility 1|
When using the FVB/NJ mouse strain in a publication, please include JAX stock #001800 in your Materials and Methods section.
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