Mice bearing the non-allelic mutations 1pr and gld develop massive lymphoproliferation and autoimmunity. Phenotypic and functional studies of lymphocytes from gld homozygotes showed that they had many abnormalities in common with mice homozygous for the 1pr mutation. These two mutations may affect different enzymes in a single metabolic pathway of major importance to T cell development. SJL/J mice homozygous for the 1pr mutation were found to die with progressive lung disease and their lymphocytes expressed high levels of infectious ecotropic murine leukemia viruses. Mice of this strain heterozygous for 1pr died with accelerated B cell lineage lymphomas. An effect of 1pr in the heterozygous state on disease was not seen in other strains of mice. Enhanced virus expression in 1pr mice was not related to linkage between 1pr and one of the two endogenous ecotropic proviruses.
