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Infection of baby hamster kidney cells with vesicular stomatitis virus (VSV) results in the accumulation of immature U1 and U2 small nuclear ribonucleoproteins (snRNPs) that contain precursor U RNAs and at least some of the proteins specific for U1 and U2 snRNAs but lack the Sm complex of proteins that is common to these U snRNAs. The VSV function required for this effect is not known, but direct inhibition of cellular transcription did not alter the maturation of U1 and U2 snRNPs. On the other hand, viral transcription but not viral translation was required to inhibit U1 and U2 snRNP maturation. Temperature shift experiments with the mutant G114 showed that ongoing viral transcription was necessary, but that viral mRNA was not required for this inhibition. Furthermore, the VSV function involved in the inhibition of maturation of U1 and U2 snRNPs had a small UV target size of approximately 10 to 20 nucleotides. We demonstrate that temperature-sensitive mutants of VSV can be used as a tool to initiate the assembly of snRNPs in infected cells. These results are compatible with the suggestion that perturbation of snRNP metabolism by VSV precedes and is distinct from the effect of VSV on cellular RNA synthesis, although VSV leader RNA may be involved in both these functions.

Viral transcription is necessary and sufficient for vesicular stomatitis virus to inhibit maturation of small nuclear ribonucleoproteins