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Poly(A)‐dependent transcription termination does not require poly(A) site cleavage (947.1)

Termination of transcription by RNA polymerase II, for genes encoding polyadenylated mRNA, requires a functional poly(A) signal in the nascent RNA. Since the poly(A) signal is best known for 3'‐end processing of RNA by cleavage and polyadenylation, it was assumed early on that the requirement of a poly(A) signal for termination reflects a need to cleave the transcript at the poly(A) site. Cleavage was proposed to provide entry for a 5’ to 3’ exonuclease that would be targeted to the elongating polymerase by degrading the nascent transcript. Subsequent discovery of the exonuclease Rat1/Xrn2, and the finding that it did indeed participate in PDT, led to almost universal acceptance of this view, which was dubbed the torpedo model. However, a number of results over the years have raised doubts about the torpedo model by suggesting that PDT can occur without cleavage at the poly(A) site‐‐‐an absolute requirement of the torpedo model. We undertook to examine definitively the validity of the torpedo model. To this end we developed an assay in which PDT and pre‐mRNA 3’‐end cleavage activities can be measured simultaneously in Hela nuclear extract. Using this assay, we have established unequivocally that cleavage at the poly(A) site is not a prerequisite for PDT. Therefore, the torpedo model cannot be correct. Moreover, we showed that PDT can be inhibited by α‐amanitin, which binds to the trigger loop in the active site of RNA polymerase II. Other methods of stopping transcription do not interfere with PDT, suggesting that it is not simply the inhibition of transcription, but an effect of α‐amanitin on the conformation of the polymerase active site that blocks PDT. Thus, neither cleavage at the poly(A) site nor degradation of the 3’ flanking RNA are required for PDT. Rather, a conformational change within the polymerase is required, presumably triggered by the apparatus that assembles on the poly(A) signal.