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High-resolution mapping of transcribing RNAPII by CRAC in a wt or a sen1T1623E mutant

ABSTRACT: High-resolution mapping of transcribing RNAPII by CRAC in a wt or a sen1T1623E mutant

PROVIDER: PRJNA730814 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14577474.fastq.gz	Fastqsanger.gz
	SRR14577475.fastq.gz	Fastqsanger.gz
	SRR14577476.fastq.gz	Fastqsanger.gz
	SRR14577477.fastq.gz	Fastqsanger.gz

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Similar Datasets

High-resolution mapping of transcribing RNAPII by CRAC in a wt or a sen1T1623E mutant

Project description:Manuscript title: Modulated termination of non-coding transcription partakes in the regulation of gene expression Here we report high-resolution analyses of transcribing RNAPII in either a wild-type (WT) background or a sen1T1623E mutant, which harbours a substitution that mimics the phosphorylation at threonine 1623. Sen1 is a well-characterized transcription termination factor for RNAPII-dependent non-coding genes in budding yeast. Here we show that the T1623E phosphomimetic mutation induces moderate but widespread termination defects at target non-coding genes, strongly suggesting that phosphoryation at T1623 modulates negatively Sen1 transcription termination activity.

2021-10-31 | GSE174623 | GEO

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

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

| PRJNA575895 | ENA

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 Pol III by CRAC in the WT and C128 mutants

Project description:High-resolution mapping of transcribing Pol III by CRAC in the WT and C128 mutants

| PRJNA804707 | ENA

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

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

| PRJNA731142 | ENA

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 Pol III by CRAC in the WT and C128 mutants

Project description:Here we report high-resolution analyses of transcribing RNA polymerase III (Pol III) in a wild-type (WT) strain and three C128 mutants. C128 is the second largest subunit of Pol III, which is the key subunit to recognize termination signal. Mutating key residues in C128 interferes with transcription termination in vitro and affect yeast viability as well, raising the question that whether these mutations provoke Pol III termination defects in vivo. Here we show that C128 mutants display termination defects at most PolIII-dependent genes, indicating that the most disruptive C128 mutations indeed impair Pol III transcription termination in vivo

2023-02-01 | GSE196398 | GEO

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

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

| PRJNA731141 | ENA

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

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 | GSE138448 | 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:High-resolution mapping of transcribing RNAPIII by CRAC upon mutation of Sen1 in the G1 phase of the cell cycle [Experiment 3]

| PRJNA731143 | ENA

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