Recruitment of RNA Polymerase II by the pioneer transcription factor PHA-4
Ontology highlight
ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
SUBMITTER: Erel Levine
PROVIDER: E-GEOD-68280 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Using staged embryos, we find many more genes with poised RNA polymerase than had been observed previously in C. elegans embryos, suggesting that early embryos accumulate poised PolII, and that poising is dynamic.
2015-07-01 | GSE68280 | GEO
Project description:The role of Polycomb group (PcG) was studied on RNA Polymerase II (Pol II) pausing phenomenon. Wild type and Polycomb mutant (esc) embryos were used for ChIP-Seq experiments using Pol II and histone methylation antibodies. Enhanced Pol II occupancy was observed for thousands of genes in esc mutant embryos, including genes not known to be bound by PRC2 or having H3K27me3 associated. Most of these genes exhibit a concomitant reduction in H3K27me3 and increase in H3K4me3 at promoter-proximal regions. Silent genes lacking promoter-associated paused Pol II in wild-type embryos are converted into âpoisedâ genes with paused Pol II in esc mutants. We suggest that this conversion of silent genes into poised genes might render differentiated cell types susceptible to switches in identity in PcG mutants. ChIP-Seq data was generated for antibodies against Pol-II, H3K4me3, H3K27me3 in both wild type and esc mutant Drosophila embryos (0-2hr, 8-12hr, and 18-24hr embryos). In addition GRO-Seq data was generated for 18-24hr esc mutant embryos.
2011-06-14 | E-GEOD-28833 | biostudies-arrayexpress
Project description:Severe loss-of-function alleles of DCL1 are embryonic lethal. Defects in cell division were seen as early as the globular stage in the strong loss-of-function allele dcl1-15. Phenotypic work with dcl1-15 and the null allele dcl1-5 suggested that, in addition to the severe patterning defects, the mutants were maturing earlier than wild-type embryos. We performed global gene expression analysis of dcl1-15 and wild-type torpedo staged embryos to examine this maturation phenotype further. The results suggested that DCL1 is a heterochronic gene. Comparisons to a time series of embryo development (http://www.seedgenenetwork.net/arabidopsis) showed that the genes differentially expressed in dcl1-15 embryos behaved more like green-cotyledon stage embryos than torpedo embryos. Seeds of a DCL1/dcl1-15 plant were sown. For each wild-type sample, 300 torpedo stage embryos were selected from wild-type siblings. For each mutant replicate, 300 dcl1-15/dcl1-15 embryos were selected from the siliques of DCL1/dcl1-15 where the wild-type embryos were at the torpedo stage.
2011-02-17 | E-GEOD-24887 | biostudies-arrayexpress
Project description:Polycomb repression is tightly associated with promoter co-occupancy of poised RNA polymerase II (RNAPII) in mouse Embryonic Stem Cells (ESCs). However, it remains unclear whether poising is a specific feature of ESCs or also associated with Polycomb during cell differentiation. Here, we show that RNAPII poising at Polycomb repressed genes is found in five stages of ESC differentiation to dopaminergic neurons. We find that key transcription factor genes of non-neuronal lineages are kept silent in the neuronal lineage through Polycomb repression in co-association with poised RNAPII in the absence of DNA methylation within DNA Methylation Valleys (DMVs). This group of poised transcription factors are preferential candidate master regulators for trans-differentiation of neurons into different lineages. We conclude that RNAPII poising is a general feature of Polycomb repression and cell plasticity in pluripotent stem cells and terminally differentiated neurons.
2017-09-29 | GSE94364 | GEO
Project description:Vertebrate embryos achieve developmental competency during zygotic genome activation (ZGA) by establishing chromatin states that silence yet poise developmental genes for subsequent lineage-specific activation. Here, we reveal how developmental gene poising is established de novo in preZGA zebrafish embryos. Poising is established at promoters and enhancers that initially contain open/permissive chromatin with ‘Placeholder’ nucleosomes (bearing H2A.Z, H3K4me1, and H3K27ac), and DNA hypomethylation. Silencing is initiated by the recruitment of Polycomb Repressive Complex 1 (PRC1), and H2Aub1 deposition by catalytic Rnf2 during preZGA and ZGA stages. During postZGA, H2Aub1 enables Aebp2-containing PRC2 recruitment and H3K27me3 deposition. Notably, preventing H2Aub1 (via Rnf2 inhibition) eliminates recruitment of Aebp2-PRC2 and H3K27me3, and elicits transcriptional upregulation of certain developmental genes during ZGA. However, upregulation is independent of H3K27me3 – establishing H2Aub1 as the critical silencing modification at ZGA. Taken together, we reveal the logic and mechanism for establishing poised/silent developmental genes in early vertebrate embryos.
2022-01-04 | GSE168361 | GEO
Project description:Vertebrate embryos achieve developmental competency during zygotic genome activation (ZGA) by establishing chromatin states that silence yet poise developmental genes for subsequent lineage-specific activation. Here, we reveal how developmental gene poising is established de novo in preZGA zebrafish embryos. Poising is established at promoters and enhancers that initially contain open/permissive chromatin with ‘Placeholder’ nucleosomes (bearing H2A.Z, H3K4me1, and H3K27ac), and DNA hypomethylation. Silencing is initiated by the recruitment of Polycomb Repressive Complex 1 (PRC1), and H2Aub1 deposition by catalytic Rnf2 during preZGA and ZGA stages. During postZGA, H2Aub1 enables Aebp2-containing PRC2 recruitment and H3K27me3 deposition. Notably, preventing H2Aub1 (via Rnf2 inhibition) eliminates recruitment of Aebp2-PRC2 and H3K27me3, and elicits transcriptional upregulation of certain developmental genes during ZGA. However, upregulation is independent of H3K27me3 – establishing H2Aub1 as the critical silencing modification at ZGA. Taken together, we reveal the logic and mechanism for establishing poised/silent developmental genes in early vertebrate embryos.
2022-01-04 | GSE168360 | GEO
Project description:Vertebrate embryos achieve developmental competency during zygotic genome activation (ZGA) by establishing chromatin states that silence yet poise developmental genes for subsequent lineage-specific activation. Here, we reveal how developmental gene poising is established de novo in preZGA zebrafish embryos. Poising is established at promoters and enhancers that initially contain open/permissive chromatin with ‘Placeholder’ nucleosomes (bearing H2A.Z, H3K4me1, and H3K27ac), and DNA hypomethylation. Silencing is initiated by the recruitment of Polycomb Repressive Complex 1 (PRC1), and H2Aub1 deposition by catalytic Rnf2 during preZGA and ZGA stages. During postZGA, H2Aub1 enables Aebp2-containing PRC2 recruitment and H3K27me3 deposition. Notably, preventing H2Aub1 (via Rnf2 inhibition) eliminates recruitment of Aebp2-PRC2 and H3K27me3, and elicits transcriptional upregulation of certain developmental genes during ZGA. However, upregulation is independent of H3K27me3 – establishing H2Aub1 as the critical silencing modification at ZGA. Taken together, we reveal the logic and mechanism for establishing poised/silent developmental genes in early vertebrate embryos.
2022-01-04 | GSE168359 | GEO
Project description:Canton S flies (as wild type) were bred at 25C and tightly staged 2-hr embryos were collected after 2 times of 2-hr prelay. The embryos were aged on the apple juice plates and aged to 4-6 and 6-8 hr. For each time point, two independent Chromatin immunoprecipitation (ChIP) experiments were performed using two different antibodies and compared to two independent mock ChIPs using the corresponding pre-immune serum. One Zfh1 antibody was generated in Guinea pig against full-length Zfh1 in the Furlong laboratory, and the other was a generous gift from Dr. Ruth Lehmann. ChIPs were optimized using the enrichment of a binding site identified in a pilot experiment of Zfh1- ChIP-on-chip measured by real-time PCR as previously described. The quality of each IP was also assessed by real-time PCR. Solexa libraries were prepared according to the manufacturer's recommendations. Library quality was assessed on a 2100 Bioanalyzer system (Agilent). All samples were single-end sequenced with 36-bp reads using an Illumina Genome Analyzer IIX by the EMBL Genomics Core Facility.
2019-07-01 | E-MTAB-7422 | biostudies-arrayexpress
Project description:Condensins are multi-subunit protein complexes that regulate chromosome structure throughout cell-cycle. Metazoans contain two types of condensin complexes (I and II) with essential and distinct functions. In C. elegans a third type of condensin (IDC) functions as part of the X chromosome dosage compensation complex1,2. We mapped genome-wide binding sites of the three condensin types in C. elegans embryos. Characteristics of condensin binding are similar between condensin types. ChIP-seq profiles of C. elegans subunits of the three condensins in 3-6 replicates from mixed stage embryos, controls are included, and RNA-Seq profiles of C. elegans in 5 replicates from mixed staged embryos. Additionally, ChIP-seq profiles of the condensin II subunit KLE-2 in 6 replicates from L3 with controls, and RNA-Seq profiles of KLE-2 mutants in 3 replicates each from L3.
2013-09-16 | E-GEOD-45678 | biostudies-arrayexpress