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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).

2011-06-01 | E-GEOD-19015 | biostudies-arrayexpress

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

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High-resolution transcriptome-wide maps of Sen1 RNA-binding by CRAC

Project description:Pervasive transcription is a widespread phenomenon leading to the production of a plethora of non-coding RNAs (ncRNAs) without apparent function. Pervasive transcription poses a risk that needs to be controlled to prevent the perturbation of gene expression. In yeast, the highly conserved helicase Sen1 restricts pervasive transcription by inducing termination of non-coding transcription. However, the mechanisms underlying the specific function of Sen1 at ncRNAs are poorly understood. Here we identify a motif in an intrinsically disordered region of Sen1 that mimics the phosphorylated carboxy terminal domain (CTD) of RNA polymerase II and characterize structurally its recognition by the CTD-interacting domain of Nrd1, an RNA-binding protein that binds specific sequences in ncRNAs. In addition, we show that Sen1-dependent termination strictly requires the recognition of the Ser5-phosphorylated form of the CTD by the N-terminal domain of Sen1. Furthermore, we find that the N-terminal and the C-terminal domains of Sen1 can mediate intra-molecular interactions. Our results shed light onto the network of protein-protein interactions that control termination of non-coding transcription by Sen1.

2020-01-31 | GSE138465 | GEO

High-resolution mapping of transcribing RNAPII by CRAC in the presence of different Sen1 variants

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High-resolution mapping of transcribing RNAPIII by CRAC upon depletion of Nrd1 [Experiment 2]

Project description:Here we report high-resolution analyses of transcribing RNAPIII in either a wild-type (WT) background or a Nrd1 auxin-inducible degron (AID) strain in which Nrd1 can be rapidly depleted upon addition of the auxin analogue Indole-3-acetic acid (IAA). Nrd1 functions together with Sen1 in transcription termination at RNAPII-dependent non-coding genes. Here we show that depletion of Nrd1 does not affect transcription termination at RNAPIII-dependent genes, indicating that Nrd1 is not an RNAPIII transcription termination factor.

2022-07-13 | GSE174699 | GEO

Transcriptome-Wide Binding Sites for Components of the Saccharomyces cerevisiae Non-poly(A) termination Pathway: Nrd1, Nab3 and Sen1

Project description:We report here the transcriptome-wide distribution of yeast Rpb2, Sen1, Nrd1 and Nab3 binding sites. These data sets provide highresolution definition of non-poly(A) terminators, identify novel genes regulated by attenuation of nascent transcripts close to the promoter, and demonstrate the widespread occurrence of Nrd1-bound 3'-antisense transcripts on genes that are poorly expressed. In addition, we show that Sen1 does not cross-link to many expected ncRNAs but surprisingly binds to pre-mRNA transcripts suggesting a role in 3' end formation and/or termination. Six samples by adaptation of PAR-ClIP procedure

2011-09-08 | E-GEOD-31764 | biostudies-arrayexpress

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.

2012-11-09 | E-GEOD-39139 | biostudies-arrayexpress

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

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High-resolution mapping of transcribing RNAPIII by CRAC upon mutation or depletion of Sen1 [Experiment 1]

Project description:Here we report high-resolution analyses of transcribing RNAPIII in either a wild-type (WT) background , a sen1-3 mutant or a Sen1 auxin-inducible degron (AID) strain in which Sen1 can be rapidly depleted upon addition of the auxin analogue Indole-3-acetic acid (IAA). Sen1 is a well-characterized transcription termination factor for RNAPII-dependent genes in budding yeast. Here we show that the presence of three point mutations in sen1-3 that abrogate the interaction of Sen1 with RNAPIII, as well as the depletion of Sen1 provoke global transcription termination defects at RNAPIII-dependent genes. These results indicate that Sen1 is also a transcription termination factor for RNAPIII transcription units.

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