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The Sen1 Helicase Prevents Genome-Wide Spurious Transcription by Controlling Transcription Termination by RNAPII

ABSTRACT: It is currently believed that termination by RNAPII occurs differently depending whether a transcript contains or lacks a polyadenylation signal (PAS). By screening for factors deficient for PAS-dependent termination in an in vivo reporter assay, we identified Sen1, a putative helicase mainly known for its role in PAS-independent termination of snoRNAs. We show for the first time that Sen1 regulates transcription termination at protein-encoding genes genome-wide. As well, we show that Sen1 suppresses cryptic transcription genome-wide, besides being required for termination of most snoRNAs. We provide evidence that Sen1 controls termination through its helicase activity and by effectively recruiting to chromatin, factors implicated in PAS-dependent (Rna14 and Rat1) or PAS-independent termination (Nrd1). Importantly, we demonstrate that the effect on transcription termination of Sen1 and Nrd1, although similar, differ quantitatively and qualitatively. Our results suggest that in yeast, termination by RNAPII at protein encoding-genes makes use of redundant pathways.

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE17559 | GEO | 2010/01/01

SECONDARY ACCESSION(S): PRJNA118659

REPOSITORIES: GEO

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The Sen1 Helicase Prevents Spurious Transcription by Controlling Genome-Wide Transcription Termination by RNAPII

Project description:RNA Polymerase II (RNAPII) termination for transcripts containing a polyadenylation signal (PAS) is thought to differ mechanistically from termination for PAS-independent RNAPII transcripts such as sn(o)RNAs. In a screen for factors required for PAS-dependent termination, we identified Sen1, a putative helicase known primarily for its role in PAS-independent termination. We show that Sen1 is required for termination on hundreds of protein-coding genes and suppresses cryptic transcription from nucleosome-free regions on a genomic scale. These effects often overlap with but are also often distinct from those caused by Nrd1 depletion, which also impacts termination of protein-coding and cryptic transcripts, including many genic antisense transcripts. Sen1 controls termination through its helicase activity and stimulates recruitment of factors previously implicated in both PAS-dependent (Rna14, Rat1) and PAS-independent (Nrd1) termination. Thus, RNAPII termination for both protein-coding genes and cryptic transcripts is dependent on multiple pathways. The 2 RNAPII datasets were produced in duplicates and the Sen1 and Nrd1 datasets in triplicates (all IP/Input).

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Senataxin associates with replication forks to protect fork integrity across RNAPII transcribed genes

Project description:Here we analysed the role of yeast Senataxin (Sen1) in coordinating replication with transcription and in protecting genome integrity. Senataxin is mutated in the two severe neurodegenerative diseases AOA2 and ALS4. We show that a fraction of Sen1/Senataxin DNA/RNA helicase associates with replication forks and protects the integrity of those fork encountering highly expressed RNAPII genes. sen1 mutants accumulate aberrant DNA structures and RNA-DNA hybrids while forks clash head-on with RNAPII transcription units and counteract recombinogenic events and accumulation of checkpoint signals. Nrd1, which acts togheter with Sen1 in trascription temination, is not recruited at replication forks. nrd1 mutants does not display replication defects, high genome instability and checkpoint activation observed in sen1 mutants The Sen1 function in replication can be therefore separable from its role in RNA processing. We propose a role for Sen1/Senataxin during chromosome replication in facilitating replisome progression across RNAPII transcribed genes thus preventing DNA-RNA hybrids accumulation when forks encounter nascent transcripts on the lagging strand template. Chip on chip analysis was carried out as described (Bermejo et al., 2011), employing anti-Flag monoclonal antibody M2 (Sigma-Aldrich) Labelled probes were hybridized to Affymetrix S.cerevisiae Tiling 1.0 (P/N 900645) arrays and processed with TAS software.

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