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

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

PROVIDER: PRJNA909625 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22561500_1.fastq.gz	Fastqsanger.gz
	SRR22561500_2.fastq.gz	Fastqsanger.gz
	SRR22561501_1.fastq.gz	Fastqsanger.gz
	SRR22561501_2.fastq.gz	Fastqsanger.gz
	SRR22561502_1.fastq.gz	Fastqsanger.gz

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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 [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.

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

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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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Project description:RNA polymerase II (RNAPII) pausing release is a recently recognized checkpoint for transcriptional regulation. The biological roles of RNAPII pausing release and the mechanisms that by which extracellular signals control it are incompletely understood. Here we identify a novel mechanism by which VEGF stimulates RNAPII pausing-release through acetylation of ETS1, a master endothelial cell transcriptional regulator. In endothelial cells (ECs), ETS1 uniquely bound transcribed gene promoters and stimulated their expression by broadly increasing RNA polymerase II (RNAPII) pause release. VEGF enhanced ETS1 chromatin occupancy. Furthermore, VEGF increased ETS1 acetylation, enhancing its binding by BRD4 and thereby stimulating RNAPII pause release. This ETS1-mediated transduction of VEGF signaling to increase RNAPII pausing release was essential for EC angiogenic responses in vitro and in vivo. Together, our results define a new angiogenic pathway in which VEGF enhances ETS1-Brd4 interaction to broadly promote RNAPII pause release and drive angiogenesis.

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