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M6A facilitates transcription termination by promoting R-loop formation

ABSTRACT: m6A facilitates transcription termination by promoting R-loop formation

PROVIDER: PRJNA556884 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9667910_1.fastq.gz	Fastqsanger.gz
	SRR9667910_2.fastq.gz	Fastqsanger.gz
	SRR9667930_1.fastq.gz	Fastqsanger.gz
	SRR9667930_2.fastq.gz	Fastqsanger.gz
	SRR9667940_1.fastq.gz	Fastqsanger.gz

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m6A facilitates transcription termination by promoting R-loop formation

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

2019-10-15 | GSE134964 | GEO

Base J represses genes at the end of polycistronic gene clusters in Leishmania major by promoting RNAP II termination

Project description:Base J and H3.V promote RNA Polymerase (RNAP) II termination within polycistronic gene clusters in the kinetoplastid species Trypanosoma brucei. Although base J has been shown to promote RNAP II termination in the related kinetoplastid species Leishmania major and Leishmania tarentolae, the role of H3.V was unclear. The effect of acute J loss on mRNA transcript abundance was also unknown. We find here that H3.V does not promote transcription termination in Leishmania major, but loss of H3.V does reduce J levels. The J loss in H3.V knockout cells is not enough to result in a termination defect, which we show is due to a threshold level of J that is sufficient to promote termination. Loss of J beyond that threshold results in termination defects. Further, the decreased J in H3.V knockout cells allowed greater reduction of J by dimethyloxalylglycine (DMOG), which inhibits J synthesis, compared to wild type cells treated with DMOG, and resulted in stronger defects in RNAP II termination and cell growth. By mRNA-seq we see largely upregulation of genes near the ends of gene clusters following J loss, indicating that J represses genes near termination sites. These findings reveal a conserved role of J in promoting termination prior to the end of polycistronic gene clusters in kinetoplastid parasites and suggest that the essential nature of J is related to its role in repressing genes by promoting termination. The role of base J and H3.V in promoting RNA Polymerase II transcription termination was assessed by small RNA-seq, mRNA-seq, and strand-specific RT-PCR. Wild type cells were compared to H3.V knockout cells and to WT and H3.V knockout cells treated with dimethyloxalylglycine (DMOG) to reduce base J.

2016-07-20 | E-GEOD-77632 | biostudies-arrayexpress

R-loop dependent promoter-proximal termination ensures genome stability

Project description:R-loop dependent promoter-proximal termination ensures genome stability

| PRJNA929274 | ENA

ΔNp63-Senataxin circuit controls keratinocyte differentiation by promoting the transcriptional termination of epidermal genes

Project description:ΔNp63, a master regulator of epithelial biology, is involved in regulating epithelial stem cell function, maintaining the integrity of stratified epithelial cells and committing epidermal cells to the differentiation program. To this end, ΔNp63 exploits several direct mechanisms. Here, we elucidated a novel mechanism whereby ΔNp63 efficiently sustains the expression of epidermal differentiation genes. We show that ΔNp63 interacts with Senataxin (SETX), an RNA/DNA helicase able to resolve the R-loop intermediates over the GC-rich termination sites of coding genes. Notably, we found that SETX and ΔNp63 co-regulate a subset of genes involved in the early step of the keratinocyte differentiation program. At the molecular level, SETX physically binds the p63 DNA binding motifs present in two early epidermal differentiation genes, Keratin 1 (KRT1) and ZNF750, facilitating R-loop removal over their 3’ ends and thus promoting efficient transcriptional termination and gene expression. Remarkably, SETX loss affects the activation of the proper epidermal differentiation program in vitro and impacts epidermal layer stratification in organotypic human skin. Furthermore, we found that SETX is mutated or downmodulated in SCC and SETX gene mutation is a negative prognostic factor for cutaneous SCC patient survival. Collectively, our results unveil SETX as a novel molecular player of skin homeostasis, potentially involved in hyperproliferative skin disorders.

2022-01-10 | GSE193205 | GEO

RNF8 ubiquitylation of XRN2 facilitates R-loop resolution and restrains genomic instability in BRCA1 mutant cells

Project description:Breast cancer linked with BRCA1/2 mutations commonly recur and resist current therapies, including PARP inhibitors. Given the lack of effective targeted therapies for BRCA1-mutant cancers, we sought to identify novel targets to selectively kill these cancers. Here, we report that loss of RNF8 significantly protects Brca1-mutant mice against mammary tumorigenesis. RNF8 deficiency in human BRCA1-mutant breast cancer cells was found to promote R-loop accumulation and replication fork instability, leading to increased DNA damage, senescence, and synthetic lethality. Mechanistically, RNF8 interacts with XRN2, which is crucial for transcription termination and R-loop resolution. We report that RNF8 ubiquitylates XRN2 to facilitate its recruitment to R-loop-prone genomic loci and that RNF8 deficiency in BRCA1-mutant breast cancer cells decreases XRN2 occupancy at R-loop-prone sites, thereby promoting R-loop accumulation, transcription-replication collisions, excessive genomic instability, and cancer cell death. Collectively, our work identifies a synthetic lethal interaction between RNF8 and BRCA1, which is mediated by a pathological accumulation of R-loops.

2023-09-14 | GSE202723 | GEO

R-loop dependent promoter-proximal termination ensures genome stability [ChIP-seq]

Project description:R-loop dependent promoter-proximal termination ensures genome stability [ChIP-seq]

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R-loop dependent promoter-proximal termination ensures genome stability [CUT&Tag]

Project description:R-loop dependent promoter-proximal termination ensures genome stability [CUT&Tag]

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R-loop dependent promoter-proximal termination ensures genome stability [ATAC-seq]

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R-loop dependent promoter-proximal termination ensures genome stability [PRO-seq]

Project description:R-loop dependent promoter-proximal termination ensures genome stability [PRO-seq]