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Intrinsic and extrinsic mechanisms cooperate to ensure efficient termination of RNAPIII transcription.

ABSTRACT: Intrinsic and extrinsic mechanisms cooperate to ensure efficient termination of RNAPIII transcription.

PROVIDER: PRJNA731364 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14587013.fastq.gz	Fastqsanger.gz
	SRR14587014.fastq.gz	Fastqsanger.gz
	SRR14587015.fastq.gz	Fastqsanger.gz
	SRR14587016.fastq.gz	Fastqsanger.gz
	SRR14587017.fastq.gz	Fastqsanger.gz

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Intrinsic and extrinsic mechanisms cooperate to ensure efficient termination of RNAPIII transcription.

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-07-13 | GSE174738 | GEO

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

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.

2022-07-13 | GSE174698 | GEO

High-resolution mapping of transcribing RNAPIII by CRAC upon mutation of Sen1 in the G1 phase of the cell cycle [Experiment 3]

Project description:Here we report high-resolution analyses of transcribing RNAPIII in either a wild-type (WT) background or a sen1-3 mutant in the G1 phase of the cell cycle. The mutations in Sen1-3 prevent the interaction of Sen1 with both RNAPIII and the replisome, raising the question whether the role of Sen1 in RNAPIII transcription termination could depend on the association of Sen1 with the replisome. Our data show that in the G1 phase of the cell cycle, where the replisome is not assembled, the sen1-3 mutant also exhibits transcription termination defects at RNAPIII-dependent genes, as in asynchronous cells. This result indicates that the role of Sen1 in termination at RNAPIII-dependent genes is independent on the association of Sen1 with the replisome.

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Sen1 and Rrm3 ensure permissive topological conditions for replication termination

Project description:Sen1 and Rrm3 ensure permissive topological conditions for replication termination

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Sen1 and Rrm3 ensure permissive topological conditions for replication termination [ChIP-chip]

Project description:Sen1 and Rrm3 ensure permissive topological conditions for replication termination [ChIP-chip]

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Sen1 and Rrm3 ensure permissive topological conditions for replication termination [ChIP-seq]

Project description:Sen1 and Rrm3 ensure permissive topological conditions for replication termination [ChIP-seq]

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Cutoff suppresses RNA polymerase II termination to ensure expression of piRNA precursors

Project description:Small non-coding RNAs called piRNAs serve as the sequence-specific guides for an adaptable immune system that represses transposable elements in germ cells of Metazoa. The adaptation of the piRNA pathway to novel transposons is believed to occur when active transposons integrate into piRNA clusters, special genomic regions, which encode piRNA precursors. In Drosophila the RDC complex, composed of Rhino, Deadlock and Cutoff (Cuff) binds chromatin of dual-strand piRNA clusters and is required for transcription of piRNA precursors, though the mechanism by which RDC license transcription remained unknown. Here we show that Cuff prevents premature termination of RNA polymerase II by two distinct mechanisms. First, Cuff prevents cleavage of nascent RNA at poly(A) sites by interfering with recruitment of the cleavage and polyadenylation specificity factor (CPSF) complex. Second, if processing does occur, Cuff protects processed transcripts from degradation by the exonuclease Rat1. Our work reveals a conceptually novel mechanism of transcriptional enhancement. In contrast to other factors that regulate termination by binding to specific signals on nascent RNA, the RDC complex inhibits termination in a chromatin-dependent and sequence-independent manner.

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Sen1 and Rrm3 ensure permissive topological conditions for replication termination [ChIP-seq]

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Sen1 and Rrm3 ensure permissive topological conditions for replication termination [ChIP-chip]

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