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Comparative transcriptome analysis of basal gene expression in Wild-type and Sen1ΔN mutant of Saccharomyces cerevisiae

ABSTRACT: In Saccharomyces cerevisiae, Sen1 is a 252-kDa, nuclear superfamily-1 RNA/DNA helicase that encoded by an essential gene SEN1 (Senataxin). It is an important component of the Nrd1p-Nab3p-Sen1p (NRD1) complex that regulates the transcriptional termination of most non-coding and some coding transcripts at RNA polymerase pause sites. Sen1 specifically interacts with Rnt1p (RNase III), an endoribonuclease, and with Rpb1p (Rpo21p), a subunit of RNA polymerase II, through its N-terminal domain (NTD), which is a critical element of the RNA-processing machinery. Moreover, mutations in the N-terminal tail of SETX, a human ortholog of yeast Senataxin (Sen1) reported in neurological disorders. In one of the earlier studies, we have reported that the loss of dispensable NTD in yeast Sen1 resulted in flocculation and slow growing phenotypes along with defective DNA damage repair mechanisms. So, we attempted to explore the molecular basis of functional impairment associated with the loss of Sen1 N-terminal domain through global oligonucleotide microarray analysis. Also, we investigated for functionally enriched pathways based on the altered basal level gene expression profiles upon NTD loss of Sen1. The microarray data were validated by quantitative real-time PCR wherever necessary.

ORGANISM(S): Schizosaccharomyces pombe Saccharomyces cerevisiae

PROVIDER: GSE75447 | GEO | 2016/10/12

SECONDARY ACCESSION(S): PRJNA304307

REPOSITORIES: GEO

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Sen1 is required for robust RNA Polymerase III transcription termination

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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.

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

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

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