Abstract
Complement-mediated cytolysis of the mouse mammary tumor virus (MMTV)-infected rat hepatoma (HTC) cell line, M1.54, resulted in recovery of a mutant derivative, designated CR5, in which the magnitude of both basal and dexamethasone-induced proviral MMTV RNA expression was selectively reduced. Variant CR5 cells were transfected with a plasmid containing the glucocorticoid-regulated MMTV promotor linked to the neomycin resistance gene (pLNL). Half-maximal resistance to G418 killing was glucocorticoid inducible in both pLNL-transfected CR5 and M1.54 cells and was dependent on glucocorticoid receptor occupancy. The down-transcription of MMTV provirus sequences cannot be conferred to transfected genes driven by the same viral promoter suggesting that CR5 cells are defective in cis acting factors. Consistent with this notion, indirect immunofluorescence of transient heterokaryons revealed that uninfected wild-type HTC cells failed to complement the defect in CR5 while CR5 cells did not suppress the wild-type phenotype of M1.54 cells.
Published Version
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