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Effect of MuLV-related genes on plasmacytomagenesis in BALB/c mice
Abstract:
The role of spreading somatic cell infections with ecotropic MuLV viruses in the induction of plasmacytomas in BALB/cAN pi mice was determined by constructing congenic mice that lacked the gene locus Cv that codes for ecotropic virus. DBA/2 mice that lack Cv on chromosome (chr) 5 carry a closely linked gene Rmcfr that determines resistance to infection with mink cell focus-forming viruses (MCF). Rmcfr was retrogressively back-crossed onto BALB/c for six successive generations to produce N6 mice. N6 mice were mated to each other to produce BALB/c.DBA/2 Rmvfr/Rmcfr homozygotes. This stock of mice lacked Cv, as demonstrated by DNA hybridization and were as fully susceptible to developing plasmacytomas as the parental BALB/c. A second congenic stock BALB/c.DBA/2 Rmcfr/Rmcfr Fv-1n/Fv-1n was also developed, but the mice of this stock showed a reduced incidence of plasmacytomas, as did BALB/c.DBA/2 Fv-1n/Fv-1n mice. These findings indicated Fv-1 or a gene closely linked to it conferred partial resistance to plasmacytomagenesis. In constructing the BALB/c.DBA/2 Fv-1n/Fv-1n stock, a "control" congenic BALB/c.DBA/2 Fv-1b/Fv-1b was also developed at N6. Surprisingly, this stock carried the Qa2+ trait. These mice were also partially resistant to plasmacytomagenesis, suggesting a gene on chromosome 17 (the location of Qa2) or a gene located elsewhere that regulates Qa2 expression is linked to a gene controlling partial resistance to plasmacytoma development.
Insights
The study investigated how ecotropic MuLV virus infections contribute to plasmacytoma development in mice. Findings suggest that the Fv-1 gene locus and potentially genes on chromosome 17 influence resistance to plasmacytomagenesis.
Area of Science:
- Immunology
- Virology
- Genetics
Background:
- Plasmacytomas are B-cell tumors often induced by retroviruses like ecotropic MuLV.
- Understanding the genetic factors influencing susceptibility to these viral infections and tumor development is crucial.
Purpose of the Study:
- To determine the role of ecotropic MuLV infections in plasmacytoma induction in BALB/c mice.
- To investigate the influence of specific gene loci (Cv, Rmcfr, Fv-1, Qa2) on plasmacytomagenesis.
Main Methods:
- Construction of congenic mouse strains lacking specific gene loci (Cv, Rmcfr, Fv-1).
- Back-crossing and breeding strategies to generate homozygous congenic mice.
- DNA hybridization to confirm gene absence.
- Monitoring plasmacytoma incidence in different congenic strains.
Main Results:
- Mice lacking the Cv gene locus remained fully susceptible to plasmacytomas.
- Mice with the Fv-1n allele (or a linked gene) showed reduced plasmacytoma incidence.
- Congenic mice carrying the Qa2+ trait also exhibited partial resistance to plasmacytomagenesis.
Conclusions:
- The Fv-1 gene or a closely linked gene confers partial resistance to plasmacytomagenesis.
- A gene on chromosome 17, or a regulator of Qa2 expression, may be linked to partial resistance to plasmacytoma development.