M6A-seq profiling in Xist and Xist_Del_A-repeat cell lines
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA596450 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10729976.fastq.gz | Fastqsanger.gz | |||
| SRR10729977.fastq.gz | Fastqsanger.gz | |||
| SRR10729978.fastq.gz | Fastqsanger.gz | |||
| SRR10729979.fastq.gz | Fastqsanger.gz | |||
| SRR10729980.fastq.gz | Fastqsanger.gz |
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Project description:By m6A-seq, we examined the m6A pattern on Xist and Xist_Del_A-repeat, which immediately after the A-repeat region. A-repeat deletion abolished the m6A methylation downstream the A-repeat but not the m6A peak located in Xist exon VII.
2020-02-01 | GSE142271 | GEO
Project description:XIST is a long non-coding RNA (lncRNA) that mediates transcriptional silencing of X chromosome genes. Here we show that XIST is highly methylated with at least 78 N6-methyladenosine (m6A) residues, a reversible base modification whose function in lncRNAs is unknown. We show that m6A formation in XIST, as well as cellular mRNAs, is mediated by RBM15 and its paralog RBM15B, which bind the m6A-methylation complex and recruit it to specific sites in RNA. This results in methylation of adenosines in adjacent m6A consensus motifs. Furthermore, knockdown of RBM15 and RBM15B, or knockdown of the m6A methyltransferase METTL3 impairs XIST-mediated gene silencing. A systematic comparison of m6A-binding proteins shows that YTHDC1 preferentially recognizes m6A in XIST and is required for XIST function. Additionally, artificial tethering of YTHDC1 to XIST rescues XIST-mediated silencing upon loss of m6A. These data reveal a pathway of m6A formation and recognition required for XIST-mediated transcriptional repression. Three to four biological HEK293T replicates were used to perform iCLIP of endogenous YTH proteins, RBM15, and RBM15B. Crosslinking induced truncations were identified using CIMS-CITS pipeline.
2016-09-07 | E-GEOD-78030 | biostudies-arrayexpress
Project description:We show that a deletion encompassing the entire Xist 5’ m6A region results in a modest reduction in Xist-mediated silencing.
2020-02-01 | GSE142270 | GEO
Project description:By m6A-seq, we examined the m6A pattern on Xist, which immediately after the A-repeat region. The cell line, integrating multiple copy of Xist on chr3, with m6A core machinery knockout (Wtap and Mettl3) were generated. We also profiled m6A-seq in transgenic Xist line, and observed a global reduction of m6A level, validated by m6A-LC-MS/MS. Unexpectedly, we haven’t observed reduced m6A level on Xist m6A region downstream of A-repeat in transgenic Xist line.
2019-06-17 | GSE119487 | GEO
Project description:XIST is a long non-coding RNA (lncRNA) that mediates transcriptional silencing of X chromosome genes. Here we show that XIST is highly methylated with at least 78 N6-methyladenosine (m6A) residues, a reversible base modification whose function in lncRNAs is unknown. We show that m6A formation in XIST, as well as cellular mRNAs, is mediated by RBM15 and its paralog RBM15B, which bind the m6A-methylation complex and recruit it to specific sites in RNA. This results in methylation of adenosines in adjacent m6A consensus motifs. Furthermore, knockdown of RBM15 and RBM15B, or knockdown of the m6A methyltransferase METTL3 impairs XIST-mediated gene silencing. A systematic comparison of m6A-binding proteins shows that YTHDC1 preferentially recognizes m6A in XIST and is required for XIST function. Additionally, artificial tethering of YTHDC1 to XIST rescues XIST-mediated silencing upon loss of m6A. These data reveal a pathway of m6A formation and recognition required for XIST-mediated transcriptional repression.
2016-09-07 | GSE78030 | GEO
Project description:Allelic silencing analysis for A-repeat and m6A region in mouse Xist
| PRJNA596451 | ENA
Project description:Xist, a pivotal player in X chromosome inactivation (XCI), has long been perceived as a cis-acting long noncoding RNA that binds exclusively to the inactive X chromosome (Xi). However, Xist’s ability to diffuse under select circumstances has long been documented, leading us to suspect that Xist RNA may have targets and functions beyond the Xi. Here, using female mouse embryonic stem cells (ES) and mouse embryonic fibroblasts (MEF) as a model, we demonstrate that Xist RNA indeed can spread beyond the Xi. However, its binding is limited to ~100 genes in differentiating ES and MEF cells. The target genes are diverse in function but are unified by their active chromatin status. Although active, Xist binding is associated with a downregulation of gene expression. Unlike on the Xi, Xist binding does not lead to full silencing and also does not spread beyond the target gene. Deleting Xist’s Repeat B (RepB) domain reduces Xist’s diffusion away from the Xi and inhibits Xist’s localization to autosomal targets. Nonetheless, Xist transcript lacking RepB fails to down-modulate autosomal gene expression. Altogether, our findings reveal Xist targets beyond the Xi and identify Repeat B as a crucial domain for its in-trans function.
2024-08-23 | GSE271097 | GEO
Project description:Xist, a pivotal player in X chromosome inactivation (XCI), has long been perceived as a cis-acting long noncoding RNA that binds exclusively to the inactive X chromosome (Xi). However, Xist’s ability to diffuse under select circumstances has long been documented, leading us to suspect that Xist RNA may have targets and functions beyond the Xi. Here, using female mouse embryonic stem cells (ES) and mouse embryonic fibroblasts (MEF) as a model, we demonstrate that Xist RNA indeed can spread beyond the Xi. However, its binding is limited to ~100 genes in differentiating ES and MEF cells. The target genes are diverse in function but are unified by their active chromatin status. Although active, Xist binding is associated with a downregulation of gene expression. Unlike on the Xi, Xist binding does not lead to full silencing and also does not spread beyond the target gene. Deleting Xist’s Repeat B (RepB) domain reduces Xist’s diffusion away from the Xi and inhibits Xist’s localization to autosomal targets. Nonetheless, Xist transcript lacking RepB fails to down-modulate autosomal gene expression. Altogether, our findings reveal Xist targets beyond the Xi and identify Repeat B as a crucial domain for its in-trans function.
2024-08-23 | GSE271096 | GEO
Project description:N6-methyl adenosine (m6A) is one of the most important RNA modifications involved in several biological and pathological processes, including cancer. Dysregulation of m6A has been linked with tumor initiation, progression, and metastasis of several cancer types, including colon cancer. A transcriptome of colon cancer describes the dysregulated coding and non-coding RNAs but does not reveal the mechanisms like m6A modifications that determine the post-transcriptional and pre-translational regulations. Epi-transcriptome profiling of m6A in colon cancer cell lines was performed using Methylated RNA Immunoprecipitation (MeRIP) sequencing. Overall, the study illustrates the distribution of m6A across the transcriptome of various colon cancer cell lines.
2023-12-30 | GSE240438 | GEO
Project description:The noncoding Xist RNA could mediate chromosome inaccessiblity, especially for the pre-open chromatin regions (enhancer, promoter, CTCF). However, Xist lacking the B-repeats loss the ability of closing the chromatin accessibility. ATAC-seq is consistent with the observation by ATAC-see. XR-PID denotes the Xist RNA polycomb interacting domain, including the entire B-repeats and part of C repeats.
2017-12-08 | GSE102848 | GEO