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A regulatory phosphosite on Mec1 controls RNAPII and RNAPIII occupancy during replication stress [tDNA]

ABSTRACT: A regulatory phosphosite on Mec1 controls RNAPII and RNAPIII occupancy during replication stress [tDNA]

PROVIDER: PRJNA744995 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15079981_1.fastq.gz	Fastqsanger.gz
	SRR15079981_2.fastq.gz	Fastqsanger.gz
	SRR15079982_1.fastq.gz	Fastqsanger.gz
	SRR15079982_2.fastq.gz	Fastqsanger.gz
	SRR15079983_1.fastq.gz	Fastqsanger.gz

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A regulatory phosphosite on Mec1 controls RNAPII and RNAPIII occupancy during replication stress [copy_number]

Project description:Upon replication stress, the Mec1ATR kinase triggers the downregulation of transcription, reducing the level of RNA polymerase on chromatin to facilitate replication fork progression. We identify a hydroxyurea-induced phosphorylation site at Mec1-S1991 that contributes to the eviction of RNAPII and RNAPIII during replication stress. The non-phosphorylatable mec1-S1991A mutant reduces replication fork progression genome-wide and compromises survival on hydroxyurea. This defect can be suppressed by destabilizing chromatin-bound RNAPII with a Rpb3-TAP fusion, suggesting that lethality arises from replication-transcription conflicts. Coincident with a failure to repress gene expression, highly transcribed genes like GAL1 persist at nuclear pores in mec1-S1991A cells. Consistently, we find pore proteins and several components controlling RNAPII and RNAPIII transcription are phosphorylated in a Mec1-dependent manner, suggesting that Mec1-S1991 phosphorylation limits conflicts between replication and either RNA polymerase complex. We further show that Mec1 contributes to reduced RNAPII occupancy on chromatin during an unperturbed S phase.

2021-09-08 | GSE180164 | GEO

A regulatory phosphosite on Mec1 controls RNAPII and RNAPIII occupancy during replication stress [tDNA]

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A regulatory phosphosite on Mec1 controls RNAPII and RNAPIII occupancy during replication stress [ChIP-seq]

2021-09-08 | GSE180165 | GEO

A regulatory phosphosite on Mec1 controls RNAPII and RNAPIII occupancy during replication stress

Project description:A regulatory phosphosite on Mec1 controls RNAPII and RNAPIII occupancy during replication stress

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A regulatory phosphosite on Mec1 controls RNAPII and RNAPIII occupancy during replication stress [copy_number]

Project description:A regulatory phosphosite on Mec1 controls RNAPII and RNAPIII occupancy during replication stress [copy_number]

| PRJNA746946 | ENA

A regulatory phosphosite on Mec1 controls RNAPII and RNAPIII occupancy during replication stress [ChIP-seq]

Project description:A regulatory phosphosite on Mec1 controls RNAPII and RNAPIII occupancy during replication stress [ChIP-seq]

| PRJNA746947 | ENA

A regulatory phosphosite on Mec1 controls RNAPII and RNAPIII occupancy during replication stress

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

2021-09-08 | GSE180167 | GEO

DCSV Phosphopeptidomics and Phosphosite Occupancy Profiling

Project description:Phosphopeptidomic and peptidomic profiling of dense core secretory vesicles. Phosphosite occupancy was measured by comparing non-phosphorylated peptide intensity before and after treatment by alkaline phosphatase,

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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.

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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.

2022-07-13 | GSE174698 | GEO

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