Deconvolution of ChIP-chip MBF occupancies reveals the temporal recruitment of Rep2 at the MBF-target genes
Ontology highlight
ABSTRACT:
ORGANISM(S): Schizosaccharomyces pombe
PROVIDER: GSE9912 | GEO | 2010/11/26
SECONDARY ACCESSION(S): PRJNA103903
REPOSITORIES: GEO
Similar Datasets
Project description:Deconvolution analysis using Rpb1 ChIP-chip results distinguishes the Cdc10 bindings at the Rpb1-poor loci (promoters) from those at the Rpb1-rich loci (intragenic sequences). Importantly, Res1 binding at the Rpb1-poor loci, but not at the Rpb1-rich loci, are dependent on the Cdc10 function, suggesting a distinct binding mechanism. Most Cdc10 promoter bindings at the Rpb1-poor loci are associated with the G1/S-phase genes. While Res1 or Res2 is found at both the Cdc10 promoter and intragenic binding sites, Rep2 appears to be absent at the Cdc10 promoter binding sites but present at the intragenic sites. Time-course ChIP-chip analysis demonstrates that Rep2 is temporally accumulated at the coding region of the MBF-target genes, resembling the RNAP-II occupancies. We analyzed MBF binding sites using Nimblegen arrays.
2010-11-26 | E-GEOD-9912 | biostudies-arrayexpress
Project description:Deletion of the flap loop in the Rp2 subunit of human RNAPII did not alter the ability of human RNAPII to initiate transcription or elongate the initiated transcripts in vivo and in vitro, and was also dispensable for elongation factor-mediated enhancement and inhibition of transcript elongation in vitro. ChIP:chip of wild-type and flap deletion human RNAPII revealed that the mutant RNAPII was not defective for promoter binding, initiation and elongation in vivo. Eight ChIP datasets were generated as log2(IP/input) fluorescence intensities using anti-FLAG IP of wild-type RPB2-FLAG cells in biological triplicate, anti-FLAG IP of delta-FL RPB2 FLAG cells in biological triplicate, and anti-RPB1 CTD, 8WG16 of both wild-type and delta-FL cells in biological duplicate. The two 8WG16- IP datasets were combined to measure the distribution of RPB1 signal.
2011-06-24 | E-GEOD-29734 | biostudies-arrayexpress
Project description:Cohesin is a protein complex that is essential for chromosome segregation. Cohesin regulates gene expression by insulation and chromatin domain formation with insulation factor CTCF. It was also reported that CTCF-independent cohesin-binding sites co-localize with transcription factors (TFs) for enhancer-promoter interaction. However, it is not a trivial task to assign whole-genome cohesin-binding regions into various functions. Also, the context-specific roles of cohesin-mediated interactions, especially on intragenic region, remains unsolved. To this end, we performed a comprehensive characterization of DNA-binding sites for cohesin and transcription factors (TFs) in MCF-7 cells with and without transcription stimulus. We integrated these epigenomic data with transcriptomic and chromatin interactions data to analyze context-specific cohesin function in genome-wide manner. As a result, we extracted a new subset of cohesin-binding sites named decreased intragenic cohesin sites (DICs), which were different from previous known functions of cohesin. DICs were negatively correlated with transcriptional regulation: a part of them were related to enhancer markers and “paused” RNA polymerase 2, while others contributed to chromatin architectures. The intron enriched DICs also showed chromatin de-compaction and special genomic bindings. Further conventional machine learning approach also captured similar DICs with distinguishable features. More importantly, DICs could be found in various tissues and cell lines, including cohesinopathy patient cells, to play a role in the disturbed transcription. These results suggested a novel function of cohesin on intragenic regions for gene transcription regulation.
2022-05-12 | GSE177045 | GEO
Project description:There were more enriched p300 and CBP bindings at the promoter regions in the cells expresing HSP70K71E compared to the control HEK293 cells were overexpressed with pCI1-EGFP (control) and with HSP70K71E-EGFP (mutant) and appied for ChIP-Seq.
2013-09-24 | E-GEOD-51117 | biostudies-arrayexpress
Project description:Transcription is a major contributor to genome instability.A main cause of transcription-associated instability relies on the capacity of transcription to stall replication. Such genome instability is increased in RNAPII mutants. ChIP-chips performed in asynchronous cultures showed an increase of the Rrm3 binding signal all over the genome in rpb1-1 compared to wild-type. ChIP-chip studies were perfomed with antibody against Flag-tagged Rrm3 protein in both wild-type and rpb1-1 cells.
2014-12-04 | E-GEOD-55184 | biostudies-arrayexpress
Project description:Analysis of Histone H3 Lysine 4 mono-, di- and trimethyl and the boundary protein CTCF in CD4+CD25+CD45RA+ regulatory T-cells and conventional CD4+CD25- T-cells. To investigate regulatory functions or potential new transcription start sites in Treg and Tconv cells, we investigated the associated histone modifications. Mono- and dimethylation of histone 3 lysin 4 (H3K4) were previously shown to mark enhancer regions, whereas H3K4 trimethylation generally associates with transcription start sites. At imprinted loci, binding of the insulator protein CTCF, which restricts or directs enhancer-promoter interactions, is often regulated by DNA-methylation. Therefore we performed ChIP-on-chip experiments (chromatin immunoprecipitation followed by microarray hybridization; samples were amplified with ligation mediated PCR [see label protocol for the procedure] prior to labeling) for mono- di- and trimethylation of histone 3 lysin 4 and of CTCF in expanded Treg and Tconv cells. Keywords: ChIP-on-chip ChIP-on-chip experiments for H3K4 mono-, di- and trimethyl and CTCF in CD4+CD25+CD45RA+ regulatory T-cells and conventional CD4+CD25- T-cells were co-hybridizied with the input. Three biologiacal replicates (rep1-3) were performed for every histone mark, two CTCF (rep1 and rep2).
2010-05-19 | E-GEOD-14234 | biostudies-arrayexpress
Project description:High BRE gene expression in MLL-AF9+ acute myeloid leukemia (AML) is associated with a favorable prognosis, while high MECOM expression confers a very poor prognosis. ChIP-seq and RNA-seq experiments on primary human MLL-AF9+ AML samples showed more pronounced signals in samples with high MECOM expression, explaining its high expression. Between samples from the two MLL-AF9+ AML subgroups, promoter marks were located at the same position at the MECOM locus. In contrast, intragenic active promoter marks in BRE were exclusively present in samples with outlier high BRE expression. 5’ RACE and RNA-seq showed biallelic transcription of a novel BRE transcript starting adjacent to the active promoter marks followed by downstream exons. RT-qPCR detected the novel BRE transcript in >50% of adult and childhood MLL-rearranged (n=56) but also MOZ-CBP+ AML (n=20), while it was virtually absent in other samples (n=145, p<0.0001). The novel BRE transcript and active promoter marks were also absent from large publicly available datasets, underlining the uniqueness of this novel BRE transcript. Genome-wide analyses of MLL-AF9+ samples showed abnormal intragenic H3K4me3 marks in 90 genes exclusively in high BRE samples. Of these genes, expression of exons downstream versus upstream was most discriminative for BRE. Luciferase reporter assays using the intragenic BRE promoter showed that it was transactivated by MLL-AF9. The new BRE transcript may encode a BRE isoform that lacks part of the N-terminus. Importantly, we detected a new in frame CHORD1-BRE fusion in a case with relapsed AML. The BRE fusion occurred in the same region as intragenic transcription activation in BRE in MLL-AF9+ AML. This work identifies strong abnormal intragenic transcription activation resulting in the formation of a new BRE transcript in MLL-AF9+ and MOZ-CBP+ AML. Future studies should reveal whether alternate BRE contributes to AML pathogenesis.
2017-12-20 | GSE89336 | GEO
Project description:Filamentous fungi are important producers of enzymes and secondary metabolites in the biotech industry. A relatively new but highly promising fungus for industrial production is Thermothelomyces thermophilus, which is closely related to the model fungus Neurospora crassa. Nevertheless, to fully exploit the potential of T. thermophilus, a deeper understanding of its biology is necessary. A critical aspect of the filamentous fungal life cycle is the production of asexual spores (conidia), regulated by various stimuli, including nutrient availability. Under certain submerged fermentation conditions, several filamentous fungi produce conidia, which can be detrimental to product expression. In this study, we utilized RNA-seq to map transcriptomic changes during conidia production under submerged conditions in T. thermophilus. We found that the essential genes for conidiation in Aspergillus sp. and N. crassa, fluG and fluffy (fl), are not essential for conidiation in T. thermophilus. However, we identified a transcription factor, res1, whose deletion resulted in a complete loss of conidia production under fermentation conditions. This deletion also led to increased biomass production without increasing enzyme secretion. Notably, the deletion of res1 did not affect spore production on solid media. Differential gene expression analysis between the wild type and the res1 deletion mutant revealed that res1 regulates a broad range of cellular and metabolic processes, including MAPK and spore production pathways. Overexpression of res1 caused a severe growth defect and early conidia production compared to the wild type. Using ChIP-seq, we identified 35 potential target genes of res1, including known conidiation-related genes such as acon3, MAPK genes, and transcription factors like cpc1, as well as genes with unknown functions. Overall, we identified res1 to be obligatory for submerged conidia production and lay the foundation for further work on the T. thermophilus conidiation pathway and its applications.
2024-10-28 | GSE273454 | GEO
Project description:Filamentous fungi are important producers of enzymes and secondary metabolites in the biotech industry. A relatively new but highly promising fungus for industrial production is Thermothelomyces thermophilus, which is closely related to the model fungus Neurospora crassa. Nevertheless, to fully exploit the potential of T. thermophilus, a deeper understanding of its biology is necessary. A critical aspect of the filamentous fungal life cycle is the production of asexual spores (conidia), regulated by various stimuli, including nutrient availability. Under certain submerged fermentation conditions, several filamentous fungi produce conidia, which can be detrimental to product expression. In this study, we utilized RNA-seq to map transcriptomic changes during conidia production under submerged conditions in T. thermophilus. We found that the essential genes for conidiation in Aspergillus sp. and N. crassa, fluG and fluffy (fl), are not essential for conidiation in T. thermophilus. However, we identified a transcription factor, res1, whose deletion resulted in a complete loss of conidia production under fermentation conditions. This deletion also led to increased biomass production without increasing enzyme secretion. Notably, the deletion of res1 did not affect spore production on solid media. Differential gene expression analysis between the wild type and the res1 deletion mutant revealed that res1 regulates a broad range of cellular and metabolic processes, including MAPK and spore production pathways. Overexpression of res1 caused a severe growth defect and early conidia production compared to the wild type. Using ChIP-seq, we identified 35 potential target genes of res1, including known conidiation-related genes such as acon3, MAPK genes, and transcription factors like cpc1, as well as genes with unknown functions. Overall, we identified res1 to be obligatory for submerged conidia production and lay the foundation for further work on the T. thermophilus conidiation pathway and its applications.
2024-10-28 | GSE273453 | GEO
Project description:Filamentous fungi are important producers of enzymes and secondary metabolites in the biotech industry. A relatively new but highly promising fungus for industrial production is Thermothelomyces thermophilus, which is closely related to the model fungus Neurospora crassa. Nevertheless, to fully exploit the potential of T. thermophilus, a deeper understanding of its biology is necessary. A critical aspect of the filamentous fungal life cycle is the production of asexual spores (conidia), regulated by various stimuli, including nutrient availability. Under certain submerged fermentation conditions, several filamentous fungi produce conidia, which can be detrimental to product expression. In this study, we utilized RNA-seq to map transcriptomic changes during conidia production under submerged conditions in T. thermophilus. We found that the essential genes for conidiation in Aspergillus sp. and N. crassa, fluG and fluffy (fl), are not essential for conidiation in T. thermophilus. However, we identified a transcription factor, res1, whose deletion resulted in a complete loss of conidia production under fermentation conditions. This deletion also led to increased biomass production without increasing enzyme secretion. Notably, the deletion of res1 did not affect spore production on solid media. Differential gene expression analysis between the wild type and the res1 deletion mutant revealed that res1 regulates a broad range of cellular and metabolic processes, including MAPK and spore production pathways. Overexpression of res1 caused a severe growth defect and early conidia production compared to the wild type. Using ChIP-seq, we identified 35 potential target genes of res1, including known conidiation-related genes such as acon3, MAPK genes, and transcription factors like cpc1, as well as genes with unknown functions. Overall, we identified res1 to be obligatory for submerged conidia production and lay the foundation for further work on the T. thermophilus conidiation pathway and its applications.
2024-10-28 | GSE273452 | GEO