Genome-wide determination of transcription start sites reveals new insights into promoter structures in the actinomycete Corynebacterium glutamicum

Abstract We report the genome-wide identification of estrogen receptor α (ERα)-binding regions in mouse liver using a combination of chromatin immunoprecipitation and tiled microarrays that cover all nonrepetitive sequences in the mouse genome. This analysis identified 5568 ERα-binding regions. In agreement with what has previously been reported for human cell lines, many ERα-binding regions are located far away from transcription start sites; approximately 40% of ERα-binding regions are located within 10 kb of annotated transcription start sites. Almost 50% of ERα-binding regions overlap genes. The majority of ERα-binding regions lie in regions that are evolutionarily conserved between human and mouse. Motif-finding algorithms identified the estrogen response element, and variants thereof, together with binding sites for activator protein 1, basic-helix-loop-helix proteins, ETS proteins, and Forkhead proteins as the most common motifs present in identified ERα-binding regions. To correlate ERα binding to the promoter of specific genes, with changes in expression levels of the corresponding mRNAs, expression levels of selected mRNAs were assayed in livers 2, 4, and 6 h after treatment with ERα-selective agonist propyl pyrazole triol. Five of these eight selected genes, Shp, Stat3, Pdgds, Pck1, and Pdk4, all responded to propyl pyrazole triol after 4 h treatment. These results extend our previous studies using gene expression profiling to characterize estrogen signaling in mouse liver, by characterizing the first step in this signaling cascade, the binding of ERα to DNA in intact chromatin.

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Dynamics of transcription-dependent H3K36me3 marking by the SETD2:IWS1:SPT6 ternary complex

10.1101/636084 ◽

2019 ◽

Cited By ~ 2

Author(s):

Katerina Cermakova ◽

Eric A. Smith ◽

Vaclav Veverka ◽

H. Courtney Hodges

Keyword(s):

Ternary Complex ◽

Spatial Distributions ◽

Epigenetic Memory ◽

Dynamic Features ◽

Transcription Start ◽

Accurate Representation ◽

Transcription Start Sites ◽

Genome Wide ◽

Genome Wide Data ◽

Tight Correlation

AbstractSETD2 contributes to gene expression by marking gene bodies with H3K36me3, which is thought to assist in the concentration of transcription machinery at the small portion of the coding genome. Despite extensive genome-wide data revealing the precise localization of H3K36me3 over gene bodies, the physical basis for the accumulation, maintenance, and sharp borders of H3K36me3 over these sites remains rudimentary. Here we propose a model of H3K36me3 marking based on stochastic transcription-dependent placement and transcription-independent spreading. Our analysis of the spatial distributions and dynamic features of these marks indicates that transcription-dependent placement dominates the establishment of H3K36me3 domains compared to transcription-independent spreading processes, and that turnover of H3K36me3 limits its capacity for epigenetic memory. By adding additional terms for asymmetric histone turnover occurring at transcription start sites, our model provides a remarkably accurate representation of H3K36me3 levels and dynamics over gene bodies. Furthermore, we validate our findings by revealing that loss of SPT6 impairs the transcription-coupled activity of the SETD2:IWS1:SPT6 ternary complex, thereby reducing the tight correlation between transcription and H3K36me3 levels at gene bodies.

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DChIPRep, an R/Bioconductor package for differential enrichment analysis in chromatin studies

10.7287/peerj.preprints.1723v2 ◽

2016 ◽

Author(s):

Christophe D Chabbert ◽

Lars M Steinmetz ◽

Bernd Klaus

Keyword(s):

Input Data ◽

Enrichment Analysis ◽

Bioconductor Package ◽

Analytic Framework ◽

Transcription Start ◽

Transcription Start Sites ◽

Genome Wide ◽

Bioconductor Project ◽

User Friendly ◽

Genome Wide Study

The genome–wide study of epigenetic states requires the integrative analysis of histone modification ChIP–seq data. Here, we introduce an easy–to–use analytic framework to compare profiles of enrichment in histone modifications around classes of genomic elements, e.g. transcription start sites (TSS). Our framework is available via the user–friendly R/Bioconductor package DChIPRep. DChIPRep uses biological replicate information as well as chromatin Input data to allow for a rigorous assessment of differential enrichment. DChIPRep is available for download through the Bioconductor project at http://bioconductor.org/packages/DChIPRep. Contact [email protected]

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RNA polymerase II-independent recruitment of SPT6L at transcription start sites in Arabidopsis

Nucleic Acids Research ◽

10.1093/nar/gkz465 ◽

2019 ◽

Vol 47 (13) ◽

pp. 6714-6725 ◽

Cited By ~ 3

Author(s):

Chen Chen ◽

Jie Shu ◽

Chenlong Li ◽

Raj K Thapa ◽

Vi Nguyen ◽

...

Keyword(s):

Rna Polymerase ◽

Rna Polymerase Ii ◽

Transcription Initiation ◽

Elongation Factor ◽

Proper Function ◽

Gene Body ◽

Transcription Start ◽

Transcription Start Sites ◽

Genome Wide ◽

Yeast Mutants

Abstract SPT6 is a conserved elongation factor that is associated with phosphorylated RNA polymerase II (RNAPII) during transcription. Recent transcriptome analysis in yeast mutants revealed its potential role in the control of transcription initiation at genic promoters. However, the mechanism by which this is achieved and how this is linked to elongation remains to be elucidated. Here, we present the genome-wide occupancy of Arabidopsis SPT6-like (SPT6L) and demonstrate its conserved role in facilitating RNAPII occupancy across transcribed genes. We also further demonstrate that SPT6L enrichment is unexpectedly shifted, from gene body to transcription start site (TSS), when its association with RNAPII is disrupted. Protein domains, required for proper function and enrichment of SPT6L on chromatin, are subsequently identified. Finally, our results suggest that recruitment of SPT6L at TSS is indispensable for its spreading along the gene body during transcription. These findings provide new insights into the mechanisms underlying SPT6L recruitment in transcription and shed light on the coordination between transcription initiation and elongation.

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GENE-58. ACTIVE TRANSCRIPTION START SITES OF MENINGIOMA SAMPLES ASSOCIATED WITH RISK OF RECURRENCE

Neuro-Oncology ◽

10.1093/neuonc/noz175.460 ◽

2019 ◽

Vol 21 (Supplement_6) ◽

pp. vi110-vi110

Author(s):

Tathiane Malta ◽

Thais Sarraf Sabedot ◽

Carlos Carlotti jr ◽

Houtan Noushmehr

Keyword(s):

Dna Methylation ◽

Recurrence Risk ◽

Transcription Start ◽

Risk Of Recurrence ◽

Transcription Start Sites ◽

Data Alignment ◽

Non Coding Rna ◽

Genome Wide ◽

Substantial Risk ◽

Active Transcription

Abstract Meningiomas are mostly benign brain tumors but have a substantial risk of recurrence, sometimes to more aggressive subtypes. Recently, a DNA methylation signature in meningioma was described as able to stratify patients by recurrence risk (favorable and unfavorable). It is well recognized that epigenetic deregulation at distinct genomic elements can affect changes in gene expression and contribute to cancer initiation and progression. Our goal for this study is to define genes that are actively expressed or repressed by both DNA methylation and chromatin histone modification (defined by H3K4me3). For this pilot study, we selected two favorable (grades I and II) and two unfavorable (grades II and III) meningioma primary tumor samples (N=4) and mapped H3K4me3 genome-wide and whole-genome DNA methylation, in an attempt to identify active transcription start sites at known promoters. After data alignment, preprocessing and peak calling, we identified 29,514 consensus peaks for H3K4me3. The differential binding analysis resulted in 5,752 H3K4me3 regions that distinguish favorable from unfavorable meningioma, mostly gain of peaks in the unfavorable group. We identified 1,505 peaks overlapping with known promoters, 51% associated with gain of peaks in the unfavorable group. Promoter-associated chromatin changes coincided with hypomethylation in 23 unique genes in the unfavorable group. Genes such as MET, PTEN, and the long non-coding RNA RP11-60L3.1 were identified as potential regulators of meningioma recurrence. Our preliminary results describe the identification of distinct genome-wide changes in chromatin associated with meningioma patient with high risk for recurrence. Identification of candidate genes will provide knowledge of the role of epigenomics in the development of malignant meningioma and of opportunities for targeted therapy.

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Genome-Wide Identification of Transcription Start Sites Yields a Novel Thermosensing RNA and New Cyclic AMP Receptor Protein-Regulated Genes in Escherichia coli

Journal of Bacteriology ◽

10.1128/jb.00398-11 ◽

2011 ◽

Vol 193 (11) ◽

pp. 2871-2874 ◽

Cited By ~ 19

Author(s):

R. Raghavan ◽

A. Sage ◽

H. Ochman

Keyword(s):

Escherichia Coli ◽

Cyclic Amp ◽

Receptor Protein ◽

Transcription Start ◽

Cyclic Amp Receptor Protein ◽

Transcription Start Sites ◽

Genome Wide

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Computational annotation of miRNA transcription start sites

Briefings in Bioinformatics ◽

10.1093/bib/bbz178 ◽

2020 ◽

Author(s):

Saidi Wang ◽

Amlan Talukder ◽

Mingyu Cha ◽

Xiaoman Li ◽

Haiyan Hu

Keyword(s):

Computational Methods ◽

Large Scale ◽

Transcription Start ◽

Protein Coding ◽

Functional Roles ◽

Transcription Start Sites ◽

Small Noncoding Rnas ◽

Mirna Genes ◽

Genome Wide ◽

Computational Annotation

Abstract Motivation MicroRNAs (miRNAs) are small noncoding RNAs that play important roles in gene regulation and phenotype development. The identification of miRNA transcription start sites (TSSs) is critical to understand the functional roles of miRNA genes and their transcriptional regulation. Unlike protein-coding genes, miRNA TSSs are not directly detectable from conventional RNA-Seq experiments due to miRNA-specific process of biogenesis. In the past decade, large-scale genome-wide TSS-Seq and transcription activation marker profiling data have become available, based on which, many computational methods have been developed. These methods have greatly advanced genome-wide miRNA TSS annotation. Results In this study, we summarized recent computational methods and their results on miRNA TSS annotation. We collected and performed a comparative analysis of miRNA TSS annotations from 14 representative studies. We further compiled a robust set of miRNA TSSs (RSmirT) that are supported by multiple studies. Integrative genomic and epigenomic data analysis on RSmirT revealed the genomic and epigenomic features of miRNA TSSs as well as their relations to protein-coding and long non-coding genes. Contact [email protected], [email protected]

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Genome-Wide Identification of Transcription Start Sites in Two Alphaproteobacteria, Rhodobacter sphaeroides 2.4.1 and Novosphingobium aromaticivorans DSM 12444

Microbiology Resource Announcements ◽

10.1128/mra.00880-20 ◽

2020 ◽

Vol 9 (36) ◽

Author(s):

Kevin S. Myers ◽

Jessica M. Vera ◽

Kimberly C. Lemmer ◽

Alexandra M. Linz ◽

Robert Landick ◽

...

Keyword(s):

Gene Expression ◽

Rhodobacter Sphaeroides ◽

Transcription Start ◽

Future Studies ◽

Transcription Start Sites ◽

Important Resource ◽

Genome Wide

ABSTRACT Here, we report the genome-wide identification of transcription start sites (TSSs) from two Alphaproteobacteria grown under conditions that result in significant changes in gene expression. TSSs that were identified as present in one condition or both will be an important resource for future studies of these, and possibly other, Alphaproteobacteria.

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