Abstract
A structural motif at the 5' end of human 7S L (srp) RNA that is recognized specifically by cellular proteins has been identified as an efficient activator of RNA polymerase (pol) III transcription in vivo and in vitro. Mutations affecting three double-stranded regions or a tetranucleotide bulge of this RNA motif result in strongly reduced expression rates. However, effective suppression is achieved by compensatory mutations restoring RNA sequence complementarity. This activation of transcription is also observed in the context of another pol III promoter and is position-dependent. The effects observed are reminiscent of the Tat-TAR trans-activation of the human immunodeficiency virus and attribute a novel function to the structure of cellular small stable RNA.
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