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Strain Name:

CPt.C3-Faslgld/J

Stock Number:

002932

Availability:

Repository- Live

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General Terms and Conditions

Former Name      CPt.C3-Tnfsf6gld/J    (Changed: 14-MAR-05 )
Genes & Alleles   Fasl;   Faslgld;

Product Information

Strain Details

Type JAX® GEMM® Strain - Congenic
Additional information on JAX® GEMM® Strains.
Type JAX® GEMM® Strain - Mutant Strain
Type JAX® GEMM® Strain - Spontaneous Mutation
Mating SystemHomozygote x Homozygote         (Female x Male)
Specieslaboratory mouse
Background Strain BALB/cAnPt
Donor Strain C3H/HeJ-Tnfsf6gld
H2 Haplotyped
GenerationN15F20+20 (21-JAN-08)

Appearance
albino
Related Genotype: A/A Tyrp1b/Tyrp1b Tyrc/Tyrc

Strain Description
Mice homozygous for the Faslgld mutation display lymphadenopathy and systemic autoimmunity similar to that in Faslpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Related Disease (OMIM) Terms

Autoimmune Lymphoproliferative Syndrome; ALPS
Mammalian Phenotype Terms assigned by genotype

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Faslgld/Faslgld

        C3H/HeJ-Faslgld/J
  • life span-post-weaning/aging
  • *normal* life span-post-weaning/aging (MGI Ref ID J:120650)
    • when placed under hyperoxic conditions for >5 days, mice do not show increased survival (resistance to hyperoxia) compared to wild-type mice
    • premature death (MGI Ref ID J:29572)
      • males survived to mean age of 396 days, females to 369 days, controls survived until 688 days
  • cardiovascular system phenotype
  • *normal* cardiovascular system phenotype (MGI Ref ID J:7306)
    • no defect detected: no vascular disease, including necrotizing arteritis or polyarteritis
  • hematopoietic system phenotype
  • abnormal T cell differentiation (MGI Ref ID J:8267)
    • abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:
    • express beta-chain of TCR
    • exhibit rearrangements of beta-chain genes
    • express TCR beta and alpha gene mRNA
    • are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+
    • bind at high levels lectins that normally bind preferentially to B cells
    • did not proliferate or generate CTL in response to stimulation with alloantigens
    • cells stimulated with Con A failed to produce IL-2
    • abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:
    • express beta-chain of TCR
    • exhibit rearrangements of beta-chain genes
    • express TCR beta and alpha gene mRNA
    • are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+
    • bind at high levels lectins that normally bind preferentially to B cells
    • did not proliferate or generate CTL in response to stimulation with alloantigens
    • cells stimulated with Con A failed to produce IL-2
  • anemia (MGI Ref ID J:7306)
    • evident in 40% of animals autopsied when moribund
  • decreased B cell number (MGI Ref ID J:29572)
    • 36 to 15%
  • enlarged spleen (MGI Ref ID J:7306)
    • evident after 13 weeks of age
    • 4-fold enlargement compared to controls
  • increased leukocyte cell number (MGI Ref ID J:7306)
    • increased lymphocyte cell number (MGI Ref ID J:29572)
      • 5-fold increase in peripheral blood lymphocytes
      • 4-fold greater than controls
      • increased T cell number (MGI Ref ID J:29572)
        • 59 to 68%
    • increased neutrophil cell number (MGI Ref ID J:7306)
      • 2-fold greater than controls
  • homeostasis/metabolism phenotype
  • skin edema (MGI Ref ID J:7306)
    • ~25% of those autopsied when moribund showed marked subcutaneous edema
  • immune system phenotype
  • abnormal T cell differentiation (MGI Ref ID J:8267)
    • abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:
    • express beta-chain of TCR
    • exhibit rearrangements of beta-chain genes
    • express TCR beta and alpha gene mRNA
    • are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+
    • bind at high levels lectins that normally bind preferentially to B cells
    • did not proliferate or generate CTL in response to stimulation with alloantigens
    • cells stimulated with Con A failed to produce IL-2
    • abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:
    • express beta-chain of TCR
    • exhibit rearrangements of beta-chain genes
    • express TCR beta and alpha gene mRNA
    • are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+
    • bind at high levels lectins that normally bind preferentially to B cells
    • did not proliferate or generate CTL in response to stimulation with alloantigens
    • cells stimulated with Con A failed to produce IL-2
  • abnormal lymph node morphology (MGI Ref ID J:7306)
    • enlarged lymph nodes (MGI Ref ID J:29572)
      • 50-fold heavier at 20 weeks of age than controls
      • enlarged peripheral lymph nodes evident at 13 weeks of age, abdominal evident shortly thereafter
      • evidence of chronic inflammation at autopsy, with proliferation of lymphocytes and admixtures of histiocytes and plasma cells observed, fibrosis and multinucleated giant cells also frequently observed
  • decreased B cell number (MGI Ref ID J:29572)
    • 36 to 15%
  • defective cytotoxic T cell cytolysis (MGI Ref ID J:17698)
    • in Fas-dependent lysis assays, but not allogeneic targets
  • enlarged spleen (MGI Ref ID J:7306)
    • evident after 13 weeks of age
    • 4-fold enlargement compared to controls
  • increased autoantibody level (MGI Ref ID J:7306)
    • thymocyte-binding autoantibody present
    • increased anti-nuclear antigen antibody level (MGI Ref ID J:7306)
      • high titers of antinuclear autoantibodies evident by 16 weeks of age in all mice assayed
      • high titers of antinuclear autoantibodies evident at 14 weeks of age
      • increased anti-double stranded DNA antibody level (MGI Ref ID J:7306)
        • high concentrations of anti-dsDNA autoantibodies present
  • increased immunoglobulin level (MGI Ref ID J:29572)
    • developed broad-based hypergammaglobulinemia
    • development of broad-based hypergammaglobulinemia
    • increased IgA level (MGI Ref ID J:7306)
      • 10-fold
    • increased IgG level (MGI Ref ID J:29572)
      • 10-fold IgG2a
      • 3- to 6-fold IgG1 and IgG2b
      • increased IgG1 level (MGI Ref ID J:7306)
      • increased IgG2a level (MGI Ref ID J:7306)
      • increased IgG2b level (MGI Ref ID J:7306)
    • increased IgM level (MGI Ref ID J:29572)
  • increased leukocyte cell number (MGI Ref ID J:7306)
    • increased lymphocyte cell number (MGI Ref ID J:29572)
      • 5-fold increase in peripheral blood lymphocytes
      • 4-fold greater than controls
      • increased T cell number (MGI Ref ID J:29572)
        • 59 to 68%
    • increased neutrophil cell number (MGI Ref ID J:7306)
      • 2-fold greater than controls
  • interstitial pneumonia (MGI Ref ID J:7306)
    • lung inflammation resembling interstitial pneumonitis evident in virtually all animals autopsied when moribund
  • renal/urinary system phenotype
  • *normal* renal/urinary system phenotype (MGI Ref ID J:7306)
    • despite glomerular deposition of immune complexes, no, or very little, glomerulonephritis was observed
  • respiratory system phenotype
  • interstitial pneumonia (MGI Ref ID J:7306)
    • lung inflammation resembling interstitial pneumonitis evident in virtually all animals autopsied when moribund
  • skin/coat/nails phenotype
  • skin edema (MGI Ref ID J:7306)
    • ~25% of those autopsied when moribund showed marked subcutaneous edema
  • tumorigenesis
  • *normal* tumorigenesis (MGI Ref ID J:108303)
    • regression of transplanted SCCVII tumors by gene therapy treatment with Il12b is normal

Faslgld/Faslgld

        B6Smn.C3-Faslgld/J
  • nervous system phenotype
  • CNS inflammation (MGI Ref ID J:120427)
    • by 7 days after TMEV infection, inflammation is present in the meninges and gray matter, but decreases by 21 days, although not as much as in controls (B6)
    • brain inflammation (MGI Ref ID J:120427)
      • by 7 days after TMEV infection, inflammation is present, decreasing slightly by 21 days, but widespread tissue damage is present, similar to controls (B6)
      • tissue damage is less frequent at 45 days than in Prf-null mice
      • at 180 days, some degree of brain pathology is still present, while inflammation is absent in controls
  • demyelination (MGI Ref ID J:120427)
    • at 45 days and later time points, there is minimal or no pathology, similar to controls and in contrast to Prf-null mice
  • immune system phenotype
  • CNS inflammation (MGI Ref ID J:120427)
    • by 7 days after TMEV infection, inflammation is present in the meninges and gray matter, but decreases by 21 days, although not as much as in controls (B6)
    • brain inflammation (MGI Ref ID J:120427)
      • by 7 days after TMEV infection, inflammation is present, decreasing slightly by 21 days, but widespread tissue damage is present, similar to controls (B6)
      • tissue damage is less frequent at 45 days than in Prf-null mice
      • at 180 days, some degree of brain pathology is still present, while inflammation is absent in controls
  • abnormal osteoclast physiology (MGI Ref ID J:127179)
    • osteoclasts are resistant to estrogen induced apoptosis
  • decreased granulocyte number (MGI Ref ID J:136745)
    • mice infected with 500 CFU of S. aureus show half the number of granulocytes infiltrate the eyes compared to infected wild-type eyes at 24 hours after infection
  • eye inflammation (MGI Ref ID J:136745)
    • mice infected with 500 CFU of S. aureus show signs of severe intraocular inflammation and tissue destruction
    • mice infected with 500 CFU of S. aureus show half the number of granulocytes infiltrate the eyes compared to infected wild-type eyes at 24 hours after infection
  • increased susceptibility to bacterial infection (MGI Ref ID J:136745)
    • mice infected with 500 CFU of S. aureus have drastically elevated number of S. aureus CFU compared to similarly-infected wild-type mice
  • increased susceptibility to viral infection (MGI Ref ID J:120427)
    • inflammation and tissue damage in the brain are slightly greater than in control, resistant mice at 45 and 180 days
  • liver inflammation (MGI Ref ID J:135830)
    • after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls
  • skeleton phenotype
  • abnormal osteoclast physiology (MGI Ref ID J:127179)
    • osteoclasts are resistant to estrogen induced apoptosis
  • decreased bone density (MGI Ref ID J:127179)
    • female mice do not lose bone density when ovaries are removed
  • vision/eye phenotype
  • abnormal eye electrophysiology (MGI Ref ID J:136745)
    • mice have only 7% of b-wave amplitude remaining at 24 hours after infection with 500CFU S. aureus, and show no detectable retinal function after this time point
  • eye inflammation (MGI Ref ID J:136745)
    • mice infected with 500 CFU of S. aureus show signs of severe intraocular inflammation and tissue destruction
    • mice infected with 500 CFU of S. aureus show half the number of granulocytes infiltrate the eyes compared to infected wild-type eyes at 24 hours after infection
  • hematopoietic system phenotype
  • decreased granulocyte number (MGI Ref ID J:136745)
    • mice infected with 500 CFU of S. aureus show half the number of granulocytes infiltrate the eyes compared to infected wild-type eyes at 24 hours after infection
  • homeostasis/metabolism phenotype
  • decreased circulating alanine transaminase level (MGI Ref ID J:135830)
    • one day following bile duct ligation (BDL), serum ALT levels are significantly lower than controls
  • liver/biliary system phenotype
  • abnormal hepatocyte morphology (MGI Ref ID J:135830)
    • confluent foci of feathery hepatocyte degeneration due to bile acid cytotoxicity are significantly reduced compared to controls 24 hours after BDL
    • decreased hepatocyte apoptosis (MGI Ref ID J:135830)
      • hepatocyte cell death is reduced compared to controls after BDL
  • focal hepatic necrosis (MGI Ref ID J:135830)
    • necroinflammatory foci after BDL are reduced in number compared to controls after BDL
  • liver inflammation (MGI Ref ID J:135830)
    • after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls

Faslgld/Faslgld

        C3H/HeJ-Faslgld
  • hematopoietic system phenotype
  • abnormal T cell morphology (MGI Ref ID J:8267)
    • lymph node cells (T cell origin) are abnormal; cells are Ly-2-/L3T4-/surface Ig-
    • abnormal T cell proliferation (MGI Ref ID J:8267)
      • cells do not proliferate in response to stimulation with alloantigens
  • homeostasis/metabolism phenotype
  • abnormal interleukin level (MGI Ref ID J:8267)
    • stimulation with concanavalin A does not induce cells to produce Il2
  • immune system phenotype
  • abnormal T cell morphology (MGI Ref ID J:8267)
    • lymph node cells (T cell origin) are abnormal; cells are Ly-2-/L3T4-/surface Ig-
    • abnormal T cell proliferation (MGI Ref ID J:8267)
      • cells do not proliferate in response to stimulation with alloantigens
  • abnormal T cell physiology (MGI Ref ID J:8267)
    • cells do not generate CTL in response to stimulation with alloantigens
    • abnormal T cell proliferation (MGI Ref ID J:8267)
      • cells do not proliferate in response to stimulation with alloantigens
  • abnormal interleukin level (MGI Ref ID J:8267)
    • stimulation with concanavalin A does not induce cells to produce Il2
  • nervous system phenotype
  • decreased neuron apoptosis (MGI Ref ID J:124252)
    • very low levels of apoptosis (15%) compared to wild-type (60%) are seen when cortical neurons are treated with Abeta25-35 or Abeta1-40 peptides
    • neuron viability is comparable to wild-type when grown in absence of Abeta or if treated with KCN which induces necrotic cell death

Faslgld/Faslgld

        involves: C3H/HeJ * CBA
  • reproductive system phenotype
  • *normal* reproductive system phenotype (MGI Ref ID J:114219)
    • 2 days after gonadectomy, vaginal organ weight decreases by similar value as observed in wild-type, indicating normal estrogen-dependent cell death

Gene & Allele Details

Allele Symbol Faslgld
Allele Name generalized lymphoproliferative disease
Common Name(s) CD95-; FasL-; Tnfsf6gld; gld;
Strain of OriginC3H/HeJ
Gene Symbol and Name Fasl, Fas ligand (TNF superfamily, member 6)
Chromosome 1
Gene Common Name(s) APT1LG1; CD178; CD95L; Fas antigen ligand; Fas-L; Faslg; TNFSF6; Tnfsf6; generalized lymphoproliferative disease; gld; tumor necrosis factor (ligand) superfamily, member 6;
Molecular Note A T-to-C transition point mutation near the 3' end of the coding sequence causes a replacement of a highly conserved phenylalanine with a leucine at position 273 in the extracellular region of the encoded protein. [MGI Ref ID J:17445]

Control Information

  Allele   Control
 Faslgld  001026 BALB/cByJ (approximate)
   The approximate control BALB/cAnLil is no longer distributed by The Jackson Laboratory.
 
  Considerations for Choosing Controls

Genotyping Protocols

Faslgld

Colony Maintenance

Diet Information LabDiet® 5K52/5K67

Related Strains

Strains carrying   Faslgld allele
001021   B6Smn.C3-Faslgld/J
000784   C3H/HeJ-Faslgld/J
008223   NOD.C3(B6)-Faslgld /LwnJ
View Strains carrying   Faslgld     (3 strains)

Strains carrying other alleles of Fasl
003499   NOD-Tg(Ins2-Fasl)24Ach
View Strains carrying other alleles of Fasl     (1 strain)

Additional Web Information

Congenic Nomenclature

Animal Health Reports

Room Number           FGB27

Research Applications

This mouse can be used to support research in many areas including:

Faslgld related

Apoptosis Research
Extracellular Modulators

Cancer Research
Genes Regulating Growth and Proliferation

Cell Biology Research
Signal Transduction

Hematological Research

Immunology and Inflammation Research
Autoimmunity (lupus erythematosus)

Mouse/Human Gene Homologs
systemic lupus erythematosus

References

Additional References

Price and Supply Information

Strain Name: CPt.C3-Faslgld/J
Stock Number: 002932

Price Details

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Supply Details

Standard SupplyRepository-Live. A collection of over 1000 strains maintained as live colonies. Individual colonies are sized to meet current customer demand. Delivery for orders of 10 mice or less ranges on average from one to eight weeks; mice are generally shipped between four to six weeks of age with a maximum shipping age of ~nine weeks. Colony sizes do not generally support stringent age specifications for large volumes of mice; however custom orders and larger quantities of mice are easily arranged. Estimated ship dates for all orders provided within 48 hours of order placement.
Supply Notes Usually shipped between four and eight weeks of age.
This strain is included in the Mouse Mutant Resource collection.
Genomic DNA is available for this strain from the Mouse DNA Resource.
LicensingSee General Terms and Conditions below  
Control InformationView Control Information in Strain Details.

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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.
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