Antisense-ColitisModel
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB79363 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The histone variant H2A.Z, which has been reported to have both activating and repressive effects on gene expression, is known to occupy nucleosomes at the 5’ ends of protein-coding genes. We now find that H2A.Z is also significantly enriched in gene coding regions and at the 3’ ends of genes in budding yeast, where it co-localises with histone marks associated with active promoters. By comparing H2A.Z binding to global gene expression in budding yeast strains engineered so that normally unstable transcripts are abundant, we show that H2A.Z is required for normal levels of antisense transcripts as well as sense ones. High levels of H2A.Z at antisense promoters are associated with decreased antisense transcript levels when H2A.Z is deleted, indicating that H2A.Z has an activating effect on antisense transcripts. Decreases in antisense transcripts affected by H2A.Z are accompanied by increased levels of paired sense transcripts. Therefore, the effect of H2A.Z on protein coding gene expression is a reflection of its importance for normal levels of both sense and antisense transcripts. Htz1 ChIP-seq in wild-type (WT) and rrp6Δ yeast, along with negative control ChIP-seq in htz1Δ and input control. Strand-specific transcriptomic profiles of WT, htz1Δ, rrp6Δ and htz1Δrrp6Δ. Replicates are present for all samples except the negative and input control ChIP samples.
2015-01-05 | E-GEOD-54105 | biostudies-arrayexpress
Project description:Antisense oligonucleotide therapy for calmodulinopathy
| PRJNA1030420 | ENA
Project description:The histone variant H2A.Z, which has been reported to have both activating and repressive effects on gene expression, is known to occupy nucleosomes at the 5’ ends of protein-coding genes. We now find that H2A.Z is also significantly enriched in gene coding regions and at the 3’ ends of genes in budding yeast, where it co-localises with histone marks associated with active promoters. By comparing H2A.Z binding to global gene expression in budding yeast strains engineered so that normally unstable transcripts are abundant, we show that H2A.Z is required for normal levels of antisense transcripts as well as sense ones. High levels of H2A.Z at antisense promoters are associated with decreased antisense transcript levels when H2A.Z is deleted, indicating that H2A.Z has an activating effect on antisense transcripts. Decreases in antisense transcripts affected by H2A.Z are accompanied by increased levels of paired sense transcripts. Therefore, the effect of H2A.Z on protein coding gene expression is a reflection of its importance for normal levels of both sense and antisense transcripts.
2015-01-05 | GSE54105 | GEO
Project description:<p>High throughput RNA Sequencing has revealed that the human genome is widely transcribed. However, the extent of natural antisense transcription, the molecular mechanisms by which natural antisense transcripts (NATs) might affect their cognate sense genes, and the role of NATs in cancer are less well understood. Here, we use strand-specific paired-end RNA sequencing (ssRNASeq) on a cohort of 376 cancer patients covering 9 tissue types to comprehensively characterize the landscape of antisense expression. Our results reveal that greater than 60% of annotated transcripts have measureable antisense expression and the expression of sense and antisense transcript pairs is in general positively correlated. Furthermore, by studying the expression of sense/antisense pairs across tissues we identify lineage-specific, ubiquitous and cancer-specific antisense loci. Our results raise the possibility that NATs participate in the regulation of well-known tumor suppressors and oncogenes. Finally, this study provides a catalogue of cancer related genes with significant antisense transcription (oncoNAT). This resource will allow researchers to investigate the molecular mechanisms of sense/antisense regulation and further advance our understanding of their role in cancer.</p>
| phs000937 | dbGaP
Project description:Despite the prevalence of antisense transcripts in bacterial transcriptomes, little is known about how their synthesis is controlled. We report that a major function of the Escherichia coli termination factor Rho and its co-factor NusG is suppression of ubiquitous antisense transcription genome-wide. Rho binds C-rich unstructured nascent RNA (high C/G ratio) prior to its ATP-dependent dissociation of transcription complexes. NusG is required for efficient termination at minority subsets (~20%) of both antisense and sense Rho-dependent terminators with lower C/G ratio sequences. In contrast, a widely studied nusA deletion proposed to compromise Rho-dependent termination had no effect on antisense or sense Rho-dependent terminators in vivo. Global co-localization of the nucleoid-associated protein H-NS with Rho-dependent terminators and genetic interactions between hns and rho suggest that H-NS aids Rho in suppression of antisense transcription. The combined actions of Rho, NusG, and H-NS appear to be analogous to the Sen1-Nrd1-Nab3 and nucleosome systems that suppress antisense transcription in eukaryotes.
2012-11-01 | GSE41936 | GEO
Project description:Disruption of expression of SUR7 antisense in S. cerevisiae.
2010-12-22 | E-TABM-1096 | biostudies-arrayexpress
Project description:Antisense transcription is common at mammalian promoters. Previous studies have largely focused on characterizing antisense transcription initiating upstream of gene transcription start sites. Here, we systematically characterize promoter-proximal antisense transcription downstream of gene transcription starts sites in human T-47D cells, investigating the genomic context of downstream antisense transcription. We find that downstream antisense transcription is widespread, with antisense transcription initiation observed within 2 kb of 28% of gene transcription start sites. Downstream antisense transcription is correlated with many regulatory features at gene promoters despite not being categorically associated with gene activation or repression. At the downstream antisense transcription start site, DNA is accessible, is enriched for protein-associated sequences motifs, and is bound by a variety of transcription factors. Downstream antisense transcription initiates between nucleosomes regularly positioned downstream of gene transcription start sites. Those nucleosomes between gene and downstream antisense transcription start sites carry histone modifications associated with active promoters, such as H3K4me3 and H3K27ac. Strikingly, this same region is bound by chromatin remodeling complexes such as HDAC and SWI/SNF. The coincidence of transcription initiation with nucleosomes displaying promoter-associated histone marks underlies an apparent connection between antisense transcription and the chromatin environment at gene promoters. The association of chromatin remodelers at sites of downstream antisense transcription initiation suggests that antisense transcription contributes to the deposition and maintenance of these chromatin features at gene promoters.
2017-02-11 | GSE74308 | GEO
Project description:It has been suggested that lncRNAs can interact with transcriptional regulators/co-factors to form ribonucleoprotein (RNP) complexes to regulate the expression of downstream genes in the cell nucleus. To identify potential interacting proteins of MaTAR25, we used two different paired sets of biotin-labeled antisense oligonucleotides targeting MaTAR25 for native RNA antisense oligonucleotide pull-down (RAP) in 4T1 cells followed by qRT-PCR to assess pull-down efficiency. Samples were also eluted from beads for mass spectrometry isobaric tags for relative and absolute quantitative (MS-iTRAQ) analysis to identify proteins that bind to MaTAR25, and PPIB as the corresponding control. We ranked the candidate interactors based on detectable peptides above background in both pair sets of oligonucleotide pull-downs, and selected candidates with at least 2-fold enrichment compared to corresponding PPIB oligo pull-down.
2020-12-23 | PXD017398 | Pride
Project description:RAPs in control of antisense transcription in E. coli
| PRJEB31692 | ENA