Exposure of mouse kidney cells to 5,6-dichloro-1-β--ribofuranosylbenzimidazole (DRB) (75 to 300 µ) during the late phase of infection by polyoma virus resulted in nearly complete (90 to 98%) inhibition of virus RNA synthesis. Sedimentation analysis revealed that, although the synthesis of high mol. wt. (> 10S) virus RNA was inhibited in a manner parallel to that of total virus RNA, the synthesis of small (3S to 7S) virus RNA was inhibited by only 40 to 50% in the presence of DRB. As a result, virus RNA synthesized in the presence of DRB contained a peak at 3S to 7S in addition to residual high mol. wt. virus RNA. Small virus RNA from either untreated or DRB-treated cells contained three- to sixfold higher levels of transcripts from the DNA fragment which lies between the HI and I sites (58.0 to 72.2 map units) than from DNA fragments covering the rest of the virus genome. Furthermore, 80% of the small RNA which hybridized to this fragment was complementary to the L strand of virus DNA. These results suggest that L strand transcripts are initiated within the I-HI DNA fragment and that a portion of these transcripts is prematurely terminated within several hundred nucleotides of the site(s) of initiation. DRB had little effect on the synthesis of these prematurely terminated RNAs.


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