title: Epigenetic control of endogenous ecotropic virus expression in SL/Ni mice.
abstract: SL/Ni mice were found to be highly polymorphic in the expression of endogenous ecotropic virus (ETV). By selective mating of the mice with either high-virus or virus-free phenotypes, the following stably virus-positive and virus-negative sublines were obtained: SL/Ni-Eco+ and SL/Ni-Eco-, respectively. This polymorphism was produced by an epigenetic factor transmitted by SL/Ni-Eco- female mice via milk. F1 hybrids between SL/Ni-Eco- females with males of high-virus strains did not express ETV, whereas reciprocal F1 hybrids did. On the other hand, F1 mice between females of low-virus strains or of NFS mice lacking the ETV proviral genome and SL/Ni-Eco- males expressed a high level of ETV. Foster-nursing of newborn mice of high-virus strains by SL/Ni-Eco- foster-mothers or injection of pooled sera of SL/Ni-Eco mice resulted in intense inhibition of virus expression. On the contrary, nursing of SL/Ni-Eco- newborns by NFS/N foster-mothers resulted in high virus expression. These observations strongly support the hypothesis that failure to express ETV by SL/Ni-Eco- mice is due to a milk-transmitted maternal resistance factor, but probably not due to genetic heterogeneity among SL/Ni sublines. This factor caused strong, long-lasting, and selective suppression of endogenous ETV, but it did not confer resistance to exogenous infection of ETV. This activity was present also in the sera of SL/Ni-Eco- mice, since neonatal injection of the sera into high-virus strains of mice, SL/Ni-Eco+, SL/Kh, and AKR/Ms, caused strong selective suppression of ETV expression. By this procedure, the spontaneous occurrence of nonthymic lymphomas in SL/Kh mice was suppressed.
mesh_terms: D000818:Animals; D005786:Gene Expression Regulation; D007112:Immunity, Maternally-Acquired; D007942:Leukemia, Experimental / Q000235:genetics*; D051379:Mice; D008815:Mice, Inbred Strains / Q000235:genetics*; D011110:Polymorphism, Genetic; D012190:Retroviridae / Q000235:genetics*