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Pgia37BALB/cCrl
QTL Variant Detail
Nomenclature
QTL variant: Pgia37BALB/cCrl
Name: proteoglycan induced arthritis 37; BALB/cCrl
MGI ID: MGI:2656556
QTL: Pgia37  Location: unknown  Genetic Position: Chr17, Syntenic
Variant
origin
Strain of Specimen:  BALB/cCrl
Variant
description
Allele Type:    QTL
Notes

Mapping and Phenotype information for this QTL, its variants and associated markers

J:78168

Pgia37, a QTL associated with arthritis on mouse Chromosome 17 at 23 cM, was examined in a population of (BALB/cCrl x DBA/1J)F2 animals.

Parental strain BALB/cCrl is resistant to collagen-induced arthritis (CIA) and susceptible to proteoglycan-induced arthritis (PGIA) while parental strain DBA/1J is susceptible to CIA and resistant to PGIA. Surprisingly, F2 animals exhibit more severe CIA than parental DBA/1J susceptible animals.

Pgia37 shows linkage to CIA susceptibility (LOD=22), severity (LOD=17),and onset (LOD=12) from 6.5 cM - 45.3 cM on chromosome 17, and shows linkage to PGIA susceptibility (LOD=4.9), severity (LOD=6.5), and onset (LOD=5) from 17.4 cM - 24.5 cM on chromosome 17.

The H2 locus maps to Pgia37 and was analyzed for its association with CIA and PGIA. The H2q allele showed correlation to CIA onset and susceptibility with a dominant mode of inheritance, while the H2q allele showed correlation with PGIA susceptibility and onset with a codominant mode of inheritance in F2 animals.

J:89536

Linkage analysis at an average resolution of 10 cM was performed on 3 separate mouse crosses to map QTLs associated with proteoglycan-induced arthritis (PGIA) and collagen-induced arthritis (CIA).

559 (BALB/c x DBA/2)F2 MHC-matched animals and 402 (BALB/c x DBA/1J)F2 MHC-unmatched animals were analyzed for linkage to PGIA.

537 (BALB/c x DBA/1J)F2 animals were analyzed for linkage to CIA. With respect to PGIA, parental strain BALB/c is highly susceptible whereas parental strains DBA/2 and DBA/1J are fullyresistant. As expected, (BALB/c x DBA/2)F1 hybrids are resistant to PGIA, but interestingly (BALB/c x DBA/1J)F1 hybrids are susceptible to PGIA. This is unusual because the BALB/c allele typically exhibits recessive susceptibility to disease, but thisisnot the case with the cross to DBA/1J.

With respect to CIA, parental strain DBA/1J is highly susceptible whereas parental strains BALB/c and DBA/2 are fully resistant. All F1s exhibited susceptibility to CIA.

Linkage to arthritis susceptibility, LOD=21.0, designated as mCia1 in Fig 3 and assigned symbol Cia1; and PGIA (LOD=6.0) were detected at the H2 locus on mouse Chromosome 17 in the (BALB/c x DBA/1J)F2 MHC-unmatched population. The PGIA locus has been mapped in previous experiments (J:78168) and is named Pgia37.

Pgia20 mapped to distal mouse Chromosome 17 in (BALB/c x DBA/1J)F2 animals (independent of MHC), and is involved in PGIA susceptibility and severity.

References
Original:  J:78168 Adarichev VA, et al., Major histocompatibility complex controls susceptibility and dominant inheritance, but not the severity of the disease in mouse models of rheumatoid arthritis. Immunogenetics. 2002 Jun;54(3):184-92
All:  2 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
10/12/2021
MGI 6.17
The Jackson Laboratory