The CPSF phosphatase module links transcription termination to chromatin silencing

Abstract

ABSTRACTRNA-mediated chromatin silencing plays important roles in development and environmental response in many organisms. However, it is still unclear how the RNA, and/or the transcriptional processes producing them, trigger chromatin silencing. Through the study of developmental timing in plants we have found co-transcriptional RNA processing modulates a chromatin regulatory mechanism controlling quantitative expression of ArabidopsisFLOWERING LOCUS C(FLC). Here, we show that the phosphatase module of the mRNA 3’ processing CPSF complex is central to this mechanism. The phosphatase module components APRF1 (yeast Swd2/human WDR82), TOPP4 (Glc7/PP1) and LD (which we show is functionally equivalent to Ref2/PNUTS) all function genetically downstream of the CPSF-mediated cleavage and polyadenylation and are necessary for chromatin modification that results inFLCtranscriptional silencing. LD has been previously shown to stoichiometrically co-associatein vivowith the histone demethylase FLD. We show both proteins result in removal of H3K4 monomethylation in the central section of theFLClocus. This links transcription termination to delivery of chromatin modifications that then influence subsequent transcription. Thus, physical association of the CPSF phosphatase module with chromatin modifiers generates a transcription-coupled silencing mechanism. The conservation of the factors involved suggest this mechanism may be generally relevant to transcription-mediated chromatin silencing.