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Spontaneous Allele Detail
Symbol: Faslpr-cg
Name: Fas (TNF receptor superfamily member 6); lymphoproliferation complementing gld
MGI ID: MGI:1856335
Synonyms: lprcg
Gene: Fas  Location: Chr19:34290666-34327772 bp, + strand  Genetic Position: Chr19, 29.48 cM
Strain of Origin:  CBA/KlJms
Allele Type:    Spontaneous
Mutation:    Single point mutation
Mutation detailsA T-to-A transversion point mutation at coding nucleotide 737 results in replacement of a highly conserved isoleucine by asparagine at position 246 (p.I246N) in the cytoplasmic region of the encoded protein. (J:1181)
Inheritance:    Recessive
View phenotypes and curated references for all genotypes (concatenated display).
Disease models
In Structures Affected by this Mutation: 3 anatomical structures
Find Mice (IMSR)
Mouse strains and cell lines available from the International Mouse Strain Resource (IMSR)
Carrying this Mutation:  Mouse Strains: 3 strains available      Cell Lines: 0 lines available
Carrying any Fas Mutation:  53 strains or lines available
This mutation, which produces massive lymphadenopathy in homozygotes, occurred spontaneously in a subline of the inbred strain CBA/KlJms maintained at the Institute of Medical Science in Tokyo. Faslpr-cg complemented both Faslpr and the generalized lymphoproliferative disease Faslgld mutation in that double heterozygotes with either mutation had lymphadenopathy. However, further crosses showed the new mutation to be an allele at Faslpr (J:24805). Like Faslpr and Faslgld mutant homozygotes, CBA-Faslpr-cg/Faslpr-cg mutants produce antibodies to some nuclear antigens, such as dsDNA, ssDNA, and poly(ADP-ribose); however, they do not produce anti-erythrocyte antibodies. Although they exhibit lymphoid cell infiltration around blood vessels in lung, liver, and kidney, they lack the immune-complex glomerulonephritis, vasculitis, and interstitial pneumonia characteristic of Faslpr homozygotes (J:616). Faslpr-cg homozygotes on the MRL genetic background developed glomerulonephritic lesions similar to those of MRL/MpJ-Faslpr mutants, although at a lower frequency, suggesting MRL/MpJ background genes control this aspect of the disease (J:1753). Studies of Faslpr and Faslpr-cg homozygotes in athymic nude (Hfh11nu/Hfh11nu) mice show that the thymus is critical for lymphadenopathy and autoimmunity (J:582).
Original:  J:24805 Matsuzawa A, et al., A new allele of the lpr locus, lprcg, that complements the gld gene in induction of lymphadenopathy in the mouse. J Exp Med. 1990 Feb 1;171(2):519-31
All:  24 reference(s)

Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB), Gene Ontology (GO)
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last database update
MGI 6.16
The Jackson Laboratory