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SRP028384
Mus musculus
4 Downloadable Samples
Illumina HiSeq 2000
Description
This experiment was designed to indentify RNAs making direct contact with EZH2 in mouse embryonic stem cells Overall design: E14 with an integrated transgene encoding HA-EZH2 were pulsed with 4-SU, irradiated with UV, and subjected to HA immunoprecipitation.
Publication Title
PRC2 binds active promoters and contacts nascent RNAs in embryonic stem cells.
Sample Metadata Fields
Cell line, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Illumina HiSeq 2000
Description
This experiment was designed to obtain the polyA+ transcriptome in E14 ESCs Overall design: PolyA+ RNA was extracted and purified from two separate clones of E14, which were treated as biological replicate
Publication Title
PRC2 binds active promoters and contacts nascent RNAs in embryonic stem cells.
Sample Metadata Fields
Cell line, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina HiSeq 2000
Description
In this experiment, we sought to analyze how the transcriptome of WT, ?5|6, and ?5|6:7|9 cells vary during differentiation of ESCs into cervical motor neurons Overall design: 3 lines (WT, ?5|6, ?5|6:7|9)
Publication Title
CTCF establishes discrete functional chromatin domains at the Hox clusters during differentiation.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
- Illumina HiSeq 2000
Description
Naturally occurring variations of Polycomb Repressive Complex 1 (PRC1) comprise a core assembly of Polycomb group proteins and additional factors that include, surprisingly, Autism Susceptibility Candidate 2 (AUTS2). While AUTS2 is often disrupted in patients with neuronal disorders, the underlying mechanism is unclear. We investigated the role of AUTS2 as part of a previously identified PRC1 complex (PRC1-AUTS2), and in the context of neurodevelopment. In contrast to the canonical role of PRC1 in gene repression, PRC1-AUTS2 activates transcription. Biochemical studies demonstrate that the CK2 component of PRC1-AUTS2 thwarts PRC1 repressive activity and AUTS2-mediated recruitment of P300 leads to gene activation. ChIP-seq of AUTS2 shows that it regulates neuronal gene expression through promoter association. Conditional CNS targeting of Auts2 in a mouse model leads to various developmental defects. These findings reveal a natural means of subverting PRC1 activity, linking key epigenetic modulators with neuronal functions and diseases. Overall design: mRNA profiles of P1 brain from wild type mice were generated by deep sequencing
Publication Title
An AUTS2-Polycomb complex activates gene expression in the CNS.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
- Illumina HiSeq 2000
Description
ISL1 is expressed in cardiac progenitor cells and plays critical roles in cardiac lineage differentiation and heart development. Cardiac progenitor cells hold great potential for clinical and translational applications. However the mechanisms underlying ISL1 function in cardiac progenitor cells have not been fully elucidated. Here we uncover a hierarchical role of ISL1 in cardiac progenitor cells, showing that ISL1 directly regulates hundreds of potential downstream targets that are implicated in cardiac differentiation, through an epigenetic mechanism. Specifically, ISL1 promotes the demethylation of tri-methylation of histone H3K27 (H3K27me3) at the enhancers of key downstream target genes, including Myocd and Mef2c, which are core cardiac transcription factors. ISL1 physically interacts with JMJD3, a H3K27me3 demethylase, and conditional depletion of JMJD3 leads to impaired cardiac progenitor cell differentiation, phenocopying that of ISL1 depletion. Interestingly, ISL1 is not only responsible for the recruitment of JMJD3 to specific target loci during cardiac progenitor differentiation, but also modulates its demethylase activity. In conclusion, ISL1 and JMJD3 partners to alter the cardiac epigenome, instructing gene expression changes that drive cardiac differentiation. Overall design: To investigate the transcriptional effects of ISL1 binding, we performed RNA-seq on day 7 Isl1 knock-down EBs versus control EBs.
Publication Title
ISL1 and JMJD3 synergistically control cardiac differentiation of embryonic stem cells.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Drosophila melanogaster
- 4 Downloadable Samples
- Illumina Genome Analyzer
Description
RNA polymerase II is decreased on heat shock-induced genes when the CTD phosphatase Fcp1 is knocked down in Drosophila S2 cells. We examined transcriptionally-engaged Pol II genome-wide with GRO-seq to determine if other genes are similarly affected. Overall design: Two biological replicates of nascent RNA sequencing
Publication Title
Fcp1 dephosphorylation of the RNA polymerase II C-terminal domain is required for efficient transcription of heat shock genes.
Sample Metadata Fields
Cell line, Subject
View Samples- Homo sapiens
- 3 Downloadable Samples
- IlluminaHiSeq2000
Description
This experiment sought to determine the genome-wide interactome of CTCF in human cells. Overall design: PAR-CLIP seq for CTCF was performed in U2OS cells in 2 biological replicates
Publication Title
CTCF regulates the human p53 gene through direct interaction with its natural antisense transcript, Wrap53.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 2 Downloadable Samples
- Illumina HiSeq 2000
Description
SFMBT1 is a poorly characterized mammalian MBT domain-containing protein homologous to Drosophila SFMBT, a Polycomb group protein involved in epigenetic regulation of gene expression. Here, we show that SFMBT1 regulates transcription in somatic cells and during spermatogenesis through the formation of a stable complex with LSD1 and CoREST. When bound to its gene targets, SFMBT1 recruits its associated proteins and causes chromatin compaction and transcriptional repression. SFMBT1, LSD1, and CoREST share a large fraction of target genes including those encoding replication-dependent histones. Simultaneous occupancy of histone genes by SFMBT1, LSD1, and CoREST is regulated during the cell cycle and correlates with the loss of RNA polymerase II at these promoters during G2, M, and G1. The interplay between the repressive SFMBT1–LSD1–CoREST complex and RNA polymerase II contributes to the timely transcriptional regulation of histone genes in human cells. SFMBT1, LSD1, and CoREST also form a stable complex in germ cells and their chromatin binding activity is regulated during spermatogenesis. Overall design: RNA-seq in HeLaS3 cells ctrl compared to triple knockdown for SFMBT1, CoREST, and LSD1
Publication Title
SFMBT1 functions with LSD1 to regulate expression of canonical histone genes and chromatin-related factors.
Sample Metadata Fields
Cell line, Treatment
View Samples- Mus musculus
- 9 Downloadable Samples
- IlluminaHiSeq2000
Description
In this experiment, we sought to determine how PRDM14 and CBFA2T2 regulate the transcriptome of mouse embryonic stem cells Overall design: 3 KO mESC lines with 3 biological replicates for each (wild type (3), PRDM14-KO (3), CBFA2T2 (3))
Publication Title
Co-repressor CBFA2T2 regulates pluripotency and germline development.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
- IlluminaGenomeAnalyzerII
Description
The Carboxy-terminal domain (CTD) of RNA Polymerase II (RNAPII) in mammals undergoes extensive post-translational modification, which is essential for transcriptional initiation and elongation. Here, we show that the CTD of RNAPII is methylated at a single arginine (R1810) by the transcriptional co-activator CARM1. Although methylation at R1810 is present on the hyper-phosphorylated form of RNAPII in vivo, Ser-2 or Ser-5 phosphorylation inhibit CARM1 activity towards this site in vitro, suggesting that methylation occurs before transcription initiation. Mutation of R1810 results in the mis-expression of a variety of snRNAs and snoRNAs, an effect that is also observed in Carm1-/- MEFs. These results demonstrate that CTD methylation facilitates the expression of select RNAs, perhaps serving to discriminate the RNAPII-associated machinery recruited to distinct gene types. Overall design: To address the function of RNAPII methylation, we generated Raji cell lines expressing an RNA Polymerase II resistant to a-amanitin and carrying either wild-type R1810 or an arginine to alanine substitution at that same residue, abolishing R1810 methylation of the CTD. In cells cultured in a-amanitin, the a-amanitin-resistant mutants fully replaced the functions of endogenous RNAPII, allowing us to study if gene-expression is affected by the absence of R1810me
Publication Title
The C-terminal domain of RNA polymerase II is modified by site-specific methylation.
Sample Metadata Fields
No sample metadata fields
View Samples