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Splicing Factor RBM22 Broadly Affects RNA Polymerase II 5' Pausing, Elongation Rate and Termination and Prevents Genome Instability [C3'-seq]

ABSTRACT: Splicing Factor RBM22 Broadly Affects RNA Polymerase II 5' Pausing, Elongation Rate and Termination and Prevents Genome Instability [C3'-seq]

PROVIDER: PRJNA909635 | ENA |

REPOSITORIES: ENA

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Splicing Factor RBM22 Broadly Affects RNA Polymerase II 5' Pausing, Elongation Rate and Termination and Prevents Genome Instability [C3'-seq]

Project description:Splicing factors are vital for the regulation of RNA splicing, but the underlying molecular mechanisms of their involvement in transcriptional processes remain poorly understood. Here, we describe a direct role of splicing factor RBM22 in coordinating multiple steps of RNA Polymerase II (RNAPII) transcription in human cells. The RBM22 protein widely occupies the RNAPII-transcribed gene locus in the nucleus. Loss of RBM22 promotes RNAPII pause release, reduces elongation velocity and provokes transcriptional readthrough genome-wide, coupled with downstream-of-gene (DoG) transcript production and genome instability. RBM22 preferentially binds to the hyperphosphorylated, transcriptionally engaged RNAPII and coordinates its dynamics by regulating the homeostasis of the 7SK-P-TEFb complex and the association between RNAPII and SPT5 at the chromatin level. Our results uncover the multifaceted role of RBM22 in orchestrating the transcriptional program of RNAPII, and provide evidence implicating a splicing factor in both RNAPII elongation kinetics and termination control.

2024-03-10 | GSE220317 | GEO

Splicing Factor RBM22 Broadly Affects RNA Polymerase II 5' Pausing, Elongation Rate and Termination and Prevents Genome Instability

Project description:Splicing Factor RBM22 Broadly Affects RNA Polymerase II 5' Pausing, Elongation Rate and Termination and Prevents Genome Instability

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Splicing Factor RBM22 Broadly Affects RNA Polymerase II 5' Pausing, Elongation Rate and Termination and Prevents Genome Instability [ChIP-seq]

Project description:Splicing Factor RBM22 Broadly Affects RNA Polymerase II 5' Pausing, Elongation Rate and Termination and Prevents Genome Instability [ChIP-seq]

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Splicing Factor RBM22 Broadly Affects RNA Polymerase II 5' Pausing, Elongation Rate and Termination and Prevents Genome Instability [ChIP-seq]

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Splicing Factor RBM22 Broadly Affects RNA Polymerase II 5' Pausing, Elongation Rate and Termination and Prevents Genome Instability

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

2024-03-09 | GSE220318 | GEO

Replication termination is mediated by Top2 and occurs at genomic loci containing pausing elements

Project description:[original title] Chromosome replication initiates at multiple replicons and terminates when forks converge. In Escherichia coli, the Tus-TER complex mediates polar fork converging at the terminator region and aberrant termination events challenge chromosome integrity and segregation. Since in eukaryotes termination is less characterized, we used budding yeast to identify the factors assisting fork fusion at replicating chromosomes. Using genomic and mechanistic studies we have identified and characterized 71 chromosomal termination regions (TERs). TERs contain fork pausing elements that influence fork progression and merging. The Rrm3 DNA helicase assists fork progression across TERs counteracting the accumulation of X-shaped structures. The Top2 DNA topoisomerase associates at TERs in S-phase and G2/M facilitates fork fusion and prevents DNA breaks and genome rearrangements at TERs. We propose that in eukaryotes replication fork barriers, Rrm3 and Top2 coordinate replication fork progression and fusion at termination regions thus counteracting abnormal genomic transitions. Signal tracks in BED format suitable for visualization on the UCSC genome browser can be found at http://bio.ifom-ieo-campus.it/supplementary/Fachinetti_et_al_MOLCELL_2010

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Road-block transcription termination by Reb1p enforces transcription boundaries

Project description:Widely transcribed and compact genomes face the major challenge of coping with frequent overlapping or concurrent transcription events. Efficient and timely transcription termination is crucial to control pervasive transcription. In yeast, RNA polymerase II (RNAPII) termination mainly occurs via two pathways, one generating mRNAs and one dedicated to non-coding RNAs, and is triggered by signals that are recognized on the nascent RNA by a specific complex. We describe here a novel pathway of RNAPII transcription termination that is triggered by the binding to the DNA of the transcriptional activator Reb1p. We show that termination follows road-block induced pausing of RNAPII and requires ubiquitylation of RNAPII. The released RNAs are rapidly degraded, which defines a new class of cryptic unstable transcripts. We show that Reb1p-dependent termination can prevent transcriptional interference. This work reveals a novel role for Reb1p and a new paradigm for preserving the functional integrity of nucleosome free regions.

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Project description:Embryonic stem (ES) cells and embryos reversibly pause via chemical mTOR inhibition. In this study, we investigate the tissue-specific response to mTORi-induced pausing in ES and trophoblast stem (TS) cells. To resolve the sequential rewiring of the proteome, we conducted a time-series proteomics experiment at 1, 3, 6, 12, 24, and 48 hours upon induction of pausing, and at 1, 3, 6, 12, 24, and 48 hours upon release of pausing in ES and TS cells. We find that ES, but not TS cells pause reversibly. To optimise developmental pausing conditions, we reasoned that by understanding the difference in pausing response of ES and TS cells, we could identify which pathways are essential for pausing. We found that KEGG pathways related to amino acid degradation, fatty acid degradation, and DNA repair are upregulated in ES cells, but downregulated in TS cells during entry into pausing. Moreover, by targeted metabolomics, we found a depletion of short chain carnitines in the paused ES cells. To extend the length of developmental pausing, we supplemented paused embryos with L-carnitine. The L-carnitine supplementation facilitates lipid usage and prolongs the pausing length by 19 days through the establishment of a more dormant state.

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