The Paf1 complex promotes displacement of histones upon rapid induction of transcription by RNA polymerase II

Here we show that depletion of the Ctr9 or Paf1 component of the Paf1 complex delays the loss of histones from the GAL1 gene upon induction. This delay in histone removal is accompanied by a decrease in association of RNA pol II with GAL1 and altered distribution of the polymerase along the locus.These observations may explain why initial induction of GAL transcripts is reduced in Ctr9- or Paf1-deficient cells, and is consistent with a model suggesting that the Paf1 complex and the histone modifications that it mediates increase efficiency of transcriptional elongation by promoting nucleosomal destabilization and histone removal.Transcription by RNA polymerase (pol) II is subject to complex regulation at the level of chromatin modification and assembly. Several classes of chromatin modifying proteins have been identified; these contribute to gene activation by promoting chromatin decondensation, thereby allowing access of RNA pol II to regulatory sequences and facilitating movement of RNA pol II and associated factors through transcription units. ATP-dependent remodeling factors, including SWI/SNF and NURF, disrupt nucleosome structure and increase DNA accessibility [1]. Histone acetyltransferases (GNAT and MYST families) promote chromatin opening, nucleosome fluidity and protein interactions by acetylating histones at specific lysine residues [2]. Histone methyltransferases (CARM1 and MLL-families) modify histones at lysine and arginine; methylation of particular residues, for example, on histone H3 at K4 and K36, is linked to active transcription and may mark recently transcribed regions [3].Efficient transcriptional elongation through chromatin requires additional factors, including FACT, Spt6 and Asf1, which are required for histone eviction and histone redeposition [4-7]. Mutation of each of these factors is associated with inappropriate nucleosomal positioning and activation of cryptic promoters within coding regions [8-10]. FACT and Asf1 may facilitate elonga