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Alternative RNA Stuctures Formed During Transcription Depend on Elongation Rate and Modify RNA processing

ABSTRACT: Alternative RNA Stuctures Formed During Transcription Depend on Elongation Rate and Modify RNA processing

PROVIDER: PRJNA627155 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11580514_1.fastq.gz	Fastqsanger.gz
	SRR11580514_2.fastq.gz	Fastqsanger.gz
	SRR11580515_1.fastq.gz	Fastqsanger.gz
	SRR11580515_2.fastq.gz	Fastqsanger.gz
	SRR11580516_1.fastq.gz	Fastqsanger.gz

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Alternative RNA structures formed during transcription depend on elongation rate and modify RNA processing.

Project description:Most RNA processing occurs co-transcriptionally. We interrogated nascent pol II transcripts by chemical and enzymatic probing and determined how the "nascent RNA structureome" relates to splicing, A-I editing and transcription speed. RNA folding within introns and steep structural transitions at splice sites are associated with efficient co-transcriptional splicing. A slow pol II mutant elicits extensive remodeling into more folded conformations with increased A-I editing. Introns that become more structured at their 3' splice sites get co-transcriptionally excised more efficiently. Slow pol II altered folding of intronic Alu elements where cryptic splicing and intron retention are stimulated, an outcome mimicked by UV, which decelerates transcription. Slow transcription also remodeled RNA folding around alternative exons in distinct ways that predict whether skipping or inclusion is favored, even though it occurs post-transcriptionally. Hence, co-transcriptional RNA folding modulates post-transcriptional alternative splicing. In summary, the plasticity of nascent transcripts has widespread effects on RNA processing.

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Alternative RNA Stuctures Formed During Transcription Depend on Elongation Rate and Modify RNA processing

Project description:Most RNA processing occurs co-transcriptionally. We interrogated nascent pol II transcripts by chemical and enzymatic probing, and determined how the “nascent RNA structureome” relates to splicing, A-I editing and transcription speed. RNA folding within introns and steep structural transitions at splice sites are associated with efficient co-transcriptional splicing. A slow pol II mutant elicits extensive remodeling into more folded conformations with increased A-I editing. Introns that become more structured at their 3’ splice sites get co-transcriptionally excised more efficiently. Slow pol II altered folding of intronic Alu elements where cryptic splicing and intron retention are stimulated, an outcome mimicked by UV which decelerates transcription. Slow transcription also remodeled RNA folding around alternative exons in distinct ways that predict whether skipping or inclusion is favored, even though it occurs post-transcriptionally. Hence co-transcriptional RNA folding modulates post-transcriptional alternative splicing. In summary the plasticity of nascent transcripts has widespread effects on RNA processing.

2021-02-09 | GSE149018 | GEO

Field conditions modify ACD6

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Chromatin regulates alternative polyadenylation via the RNA polymerase II elongation rate

Project description:The Pol II elongation rate influences poly(A) site selection, with slow and fast Pol II derivatives causing upstream and downstream shifts, respectively, in poly(A) site utilization. In yeast, depletion of either of the histone chaperones FACT or Spt6 causes an upstream shift of poly(A) site use that strongly resembles the poly(A) profiles of slow Pol II mutant strains. Like slow Pol II mutant strains, Spt6- and FACT-depleted cells exhibit processivity defects, indicating that both Spt6 and FACT stimulate the Pol II elongation rate. Poly(A) profiles of some genes show atypical downstream shifts; this subset of genes overlaps well for FACT- or Spt6- depleted strains, but it is different from the atypical genes in Pol II speed mutant strains. In contrast, depletion of histone H3 or H4 causes a downstream shift of poly(A) sites for most genes, indicating that nucleosomes inhibit the Pol II elongation rate in vivo. Thus, chromatin-based control of the Pol II elongation rate is a potential mechanism, distinct from direct effects on the cleavage/polyadenylation machinery, to regulate alternative polyadenylation in response to genetic or environmental changes.

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RNA polymerase II elongation rate controls gene expression by alternative polyadenylation

Project description:To study the impact of the RNA polymerase II (Pol II) elongation rate on gene expression, we used CRISPR-Cas9 genome editing in S. pombe to generate a "slow" Pol II mutant with decreased elongation rate. Although the mutation is well tolerated as far as cell growth is concerned, transcriptomic analyses revealed that the slow mutant tends to terminate transcription prematurely. We distinguished two mechanisms by which premature termination affects gene expression in the slow mutant: It either (1) shortens 3'UTR, or (2) derepresses protein coding genes by prematurely terminating upstream interfering RNAs. Strikingly, the genes affected by these mechanisms are enriched for genes involved in phosphate uptake and purine synthesis, two processes essential for the maintenance of the nucleotide pool of the cell. Together with evidences that nucleotides are conditional for Pol II processive elongation, our results suggest that Pol II elongation rate acts as both sensor and effector in response to nucleotide depletion.

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Project description:Paf1C regulates RNA polymerase II progression by modulating elongation rate

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Molecular Determinants for RNA Polymerase II Elongation Rate and Acceleration

Project description:Recent studies reveal a striking phenomenon that RNA Polymerase II (Pol II) appears to travel on gene body in an accelerated fashion, but the mechanism has remained unknown. We performed synchronized transcription coupled with deep sequencing, observing an inverse relationship between initial rate and acceleration in different cell types. We directly tested several correlative events and detected a positive contribution of the splicing commitment factor SRSF2 to Pol II acceleration, suggesting a functional benefit of co-transcriptional pre-mRNA splicing in transcription elongation. Unexpectedly, we found that perturbation of Pol II Ser2 phosphorylation had little impact on Pol II elongation or acceleration. While H3K79me2 has been positively correlated with Pol II elongation, we showed that reduction of this histone modification event actually accelerated Pol II elongation. Together, these data suggest a combined effect of gradual gain-of-competence and gradual lost-of-epigenetic barriers as the mechanism for accelerated Pol II elongation. DRB time-course releasing assay under functional perturbation

2015-12-31 | E-GEOD-66021 | biostudies-arrayexpress

Paf1C regulates RNA polymerase II progression by modulating elongation rate

Project description:Elongation factor Paf1C regulates several stages of the RNA polymerase II (Pol II) transcription cycle, although it is unclear how it modulates Pol II distribution and progression in mammalian cells. We found that conditional ablation of Paf1 resulted in the accumulation of unphosphorylated and Ser5 phosphorylated Pol II around promoter proximal regions and within the first 20-30 kb of gene bodies, respectively. Paf1 ablation did not impact the recruitment of other key elongation factors, namely, Spt5, Spt6, and the FACT complex, suggesting that Paf1 function may be mechanistically distinguishable from each of these factors. Moreover, loss of Paf1 triggered an increase in TSS-proximal nucleosome occupancy, which could impose a considerable barrier to Pol II elongation past TSS-proximal regions. Remarkably, accumulation of Ser5P in the first 20-30 kb coincided with reductions in histone H2B ubiquitylation within this region. Furthermore, we show that nascent RNA species accumulate within this window, suggesting a mechanism whereby Paf1 loss leads to aberrant, prematurely terminated transcripts and diminution of full-length transcripts. Importantly, we found that loss of Paf1 results in Pol II elongation rate defects with significant rate compression. Our findings suggest that Paf1C is critical for modulating Pol II elongation rates by functioning beyond the pause-release step as an "accelerator" over specific early gene body regions.

2019-06-28 | GSE116169 | GEO

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