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SJL Mouse Inbred mouse

Model characteristics

Type:

Inbred mouse

Strain name:

SJL/JRj

Origin:

Zentralinstitut für Versuchstierzucht (Hannover) - 1988 (F109)

Colour and related genotype:

Albino mouse, A/A, Tyr^c/Tyr^c, Oca2^p/Oca2^p - MHC: Haplotype H2^s

Breeding:

Difficult to rear

Cryo

In vivo

In vitro

Description of our model and application areas

Created in 1955 by James Lambert (The Jackson Laboratory), from three sources of SWISS WEBSTER outbred stock that were brought to The Jackson Laboratory between 1938 and 1943, when brother-sister matings started.
SJL/JRj mice show a high incidence of reticulum cell sarcomas, as in Hodgkin’s disease, around year one of age. These sarcomas first appear in aggregated lymphoid nodules (Peyer’s patches) and mesenteric lymph nodes and then in the spleen and liver, the thymus and other lymph nodes. Most of these tumours are of mixed cells and classified as type B reticulum cell neoplasms but some are type A histiocytomas.

This strain is also characterized by the aggressiveness of its males and its sensitivity to experimental autoimmune encephalomyelitis (EAE) in multiple sclerosis research. It also develops spontaneous myopathy due to a mutation in the Dysferlin gene. It has been demonstrated that the Dysfm allele leads
to a decrease in the level of Dysferlin protein in SJL mice which renders them a good model for the study of Limb girdle muscular dystrophy 2B (LGMD 2B). This myopathy is characterized by a progressive loss of muscular mass and strength; muscular pathology can go as far as necrosis of the fibers and their replacement by fat. Although muscular weakness can be detected at 3 weeks of age, the greatest complications occur after 6 months of age.

SJL/JRj mice are immunocompetent, they show decreased NK activity and higher levels of circulating T cells. SJL/JRj mice are resistant to Diet-induced-obesity (DIO).

Important notices:
SJL/JRj mice are homozygous for the rd1 mutation: Pde6brd1 (phosphodiesterase 6b, retinal degeneration 1) which leads to an early onset retinal degeneration that leads to blindness. This mutation is the result of a viral insertion and a nonsense recessive mutation of the Pde6b gene’s exon 7 (Chromosome 5) which encodes the beta-subunit of rod cGMP-phosphodiesterase. This strain carries the Ptprca (=Ly5a or CD45.1) mutation (protein tyrosin phosphatase receptor type C, a variant).