In Saccharomyces cerevisiae, short noncoding RNA (ncRNA) generated by RNA 
polymerase II (Pol II) are terminated by the NRD complex consisting of Nrd1, 
Nab3, and Sen1. We now show that Pcf11, a component of the cleavage and 
polyadenylation complex (CPAC), is also generally required for NRD-dependent 
transcription termination through the action of its C-terminal domain 
(CTD)-interacting domain (CID). Pcf11 localizes downstream from Nrd1 on NRD 
terminators, and its recruitment depends on Nrd1. Furthermore, mutation of the 
Pcf11 CID results in Nrd1 retention on chromatin, delayed degradation of ncRNA, 
and restricted Pol II CTD Ser2 phosphorylation and Sen1-Pol II interaction. 
Finally, the pcf11-13 and sen1-1 mutant phenotypes are very similar, as both 
accumulate RNA:DNA hybrids and display Pol II pausing downstream from NRD 
terminators. We predict a mechanism by which the exchange of Nrd1 and Pcf11 on 
chromatin facilitates Pol II pausing and CTD Ser2-P phosphorylation. This in 
turn promotes Sen1 activity that is required for NRD-dependent transcription 
termination in vivo.