Genome-wide maps of Cbx3 in pluripotent mESC and pre-iPSCs
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Rupa Sridharan
PROVIDER: E-GEOD-44242 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Publications
Proteomic and genomic approaches reveal critical functions of H3K9 methylation and heterochromatin protein-1γ in reprogramming to pluripotency.
Sridharan Rupa R Gonzales-Cope Michelle M Chronis Constantinos C Bonora Giancarlo G McKee Robin R Huang Chengyang C Patel Sanjeet S Lopez David D Mishra Nilamadhab N Pellegrini Matteo M Carey Michael M Garcia Benjamin A BA Plath Kathrin K
Nature cell biology 20130609 7
Reprogramming of somatic cells into induced pluripotent stem cells (iPSCs) involves a marked reorganization of chromatin. To identify post-translational histone modifications that change in global abundance during this process, we have applied a quantitative mass-spectrometry-based approach. We found that iPSCs, compared with both the starting fibroblasts and a late reprogramming intermediate (pre-iPSCs), are enriched for histone modifications associated with active chromatin, and depleted for m ...[more]
Similar Datasets
Project description:We examined the locations of Cbx3 by chromatin immunoprecipitation in ESCs and pre-iPSCs
2013-06-05 | GSE44242 | GEO
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2015-08-05 | E-GEOD-70734 | biostudies-arrayexpress
Project description:Half of all human transcription factors use C2H2 zinc finger domains to specify site-specific DNA binding and yet very little is known about their role in gene regulation. Based on in vitro studies, a zinc finger code has been developed that predicts a binding motif for a particular zinc finger factor (ZNF). However, very few studies have performed genome-wide analyses of ZNF binding patterns and thus it is not clear if the binding code developed in vitro will be useful for identifying target genes of a particular ZNF. We performed genome-wide ChIP-seq for ZNF263, a C2H2 ZNF that contains 9 finger domains, a KRAB repression domain, and a SCAN domain and identified more than 5000 binding sites in K562 cells. Our results suggest that ZNF263 binds to a 24 nt site which differs from the motif predicted by the zinc finger code in several positions. Interestingly, many of the ZNF263 binding sites are located within the transcribed region of the target gene. Although ZNFs containing a KRAB domain are thought to function mainly as transcriptional repressors, many of the ZNF263 target genes are expressed at high levels. To address the biological role of ZNF263, we identified genes whose expression was altered by treatment of cells with ZNF263-specific siRNAs. Our results suggest that ZNF263 can have both positive and negative effects on transcriptional regulation of its target genes. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Examination of ZNF263 ChIP-seq in K562 cells.
2009-12-03 | E-GEOD-19235 | biostudies-arrayexpress
Project description:Vascular endothelial dysfunction underlies the genesis and progression of numerous diseases. Whereas the GATA transcription factor GATA-2 is expressed in endothelial cells and is implicated in coronary heart disease, it has been studied predominantly as a master regulator of hematopoiesis. As many questions remain unanswered regarding GATA-2 function in the vascular biology realm, we used ChIP-seq and loss-of-function strategies to define the GATA-2-instigated genetic network in human endothelial cells. By contrast to erythroid cells, GATA-2 occupied a unique target gene ensemble, consisting of genes encoding key determinants of endothelial cell identity and inflammation. GATA-2-occupied sites characteristically contained motifs that bind Activator Protein-1 (AP-1), a pivotal regulator of inflammatory genes. GATA-2 frequently occupied the same chromatin sites as c-JUN and c-FOS, heterodimeric components of AP-1. Though all three components were required for maximal AP-1 target gene expression, GATA-2 was not required for AP-1 chromatin occupancy. GATA-2 conferred maximal phosphorylation of chromatin-bound c-JUN at Ser 73, which stimulates AP-1-dependent transactivation, in a chromosomal context-dependent manner. This work establishes a link between a GATA factor and inflammation, mechanistic insights underlying GATA-2-AP-1 cooperativity, and a rigorous genetic framework for understanding GATA-2 function in normal and pathophysiological vascular states. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Examination of GATA2 ChIP-seq in HUVEC cells.
2011-08-11 | E-GEOD-29531 | biostudies-arrayexpress
Project description:The orphan nuclear receptor TR4 (human testicular receptor 4 or NR2C2) plays a pivotal role in a variety of biological and metabolic processes. With no known ligand and few known target genes, the mode of TR4 function was unclear. We report the first genome-wide identification and characterization of TR4 in vivo binding. Using chromatin immunoprecipitation followed by high throughput sequencing (ChIP-seq), we identified TR4 binding sites in 4 different human cell types and found that the majority of target genes were shared among different cells. TR4 target genes are involved in fundamental biological processes such as RNA metabolism and protein translation. In addition, we found that a subset of TR4 target genes exerts cell-type specific functions. Analysis of the TR4 binding sites revealed that less than 30% of the peaks from any of the cell types contained the DR1 motif previously derived from in vitro studies, suggesting that TR4 may be recruited to the genome via interaction with other proteins. A bioinformatics analysis of the TR4 binding sites predicted a cis regulatory module involving TR4 and ETS transcription factors. To test this prediction, we performed ChIP-seq for the ETS factor ELK4 and found that 30% of TR4 binding sites were also bound by ELK4. Motif analysis of the sites bound by both factors revealed a lack of the DR1 element, suggesting that TR4 binding at a subset of sites is facilitated through the ETS transcription factor ELK4. Further studies will be required to investigate the functional interdependence of these two factors. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf 8 total ChIP-seq datasets; four TR4 and datasets done in duplicate from 4 different cell lines; ELK4 (Sap1a) duplicate dataset done from HeLa cells; 1 ELK1 replicate in HeLa cells, 2 individual replicates for histone mod datasets from K562 cells
2010-11-15 | E-GEOD-24685 | biostudies-arrayexpress
Project description:Only a small percentage of human transcription factors (e.g. those associated with a specific differentiation program) are expressed in a given cell type. Thus, cell fate is mainly determined by cell type-specific silencing of transcription factors that drive different cellular lineages. Several histone modifications have been associated with gene silencing, including H3K27me3 and H3K9me3. We have previously shown that the two largest classes of mammalian transcription factors are marked by distinct histone modifications; homeobox genes are marked by H3K27me3 and zinc finger genes are marked by H3K9me3. Several histone methyltransferases (e.g. G9a and SETDB1) may be involved in mediating the H3K9me3 silencing mark. We have used ChIP-chip (GSE24480) and ChIP-seq to demonstrate that SETDB1, but not G9a, is associated with regions of the genome enriched for H3K9me3. A current model is that SETDB1 is recruited to specific genomic locations via interaction with the corepressor TRIM28 (KAP1), which is in turn recruited to the genome via interaction with zinc finger transcription factors that contain a Kruppel-associated box (KRAB) domain. However, specific KRAB-ZNFs that recruit TRIM28 (KAP1) and SETDB1 to the genome have not been identified. We now show that ZNF274 (a KRAB-ZNF that contains 5 C2H2 zinc finger domains), can interact with KAP1 in vitro and, using ChIP-seq, we show that ZNF274 binding sites co-localize with SETDB1, KAP1, and H3K9me3 at the 3’ ends of zinc finger genes. Knockdown of ZNF274 with siRNAs reduced the levels of KAP1 and SETDB1 recruitment to the binding sites. These studies provide the first identification of a KRAB domain-containing ZNFs that is involved in recruitment of the KAP1 and SETDB1 to the human genome. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf 7 total ChIP-seq datasets; 4 ZNF274 datasets done in duplicate from 4 different cell lines; 1 KAP1 duplicate dataset done in duplicate from K562 cells; 1 SetDB1 duplicate dataset from K562 cells; 1 H3K9me3 duplicate dataset from K562 cells
2010-11-15 | E-GEOD-24632 | biostudies-arrayexpress
Project description:A current model for the genomic recruitment of Kap1 is via its interaction with KRAB domain-containing zinc finger transcription factors. We have performed ChIP-seq for various mutant KAP1 proteins and shown that this recruitment mechanism mediates binding of KAP1 only to the 3M-CM-"M-BM-^@M-BM-^Y ends of zinc finger genes and that other factors are involved in recruiting KAP1 to promoter regions. 17 total ChIP-seq datasets; three different FLAG-KAP1 mutants, one FLAG-KAP1 wild type, and four different Input datasets from 4 different stable cell lines derived from HEK293 cells: 1 FLAG-KAP1 wild type dataset and 1 Input dataset done from HEK293 stable cells; 1 FLAG-KAP1 HP1BDmut dataset and 1 Input dataset done from HEK293 stable cells, 1 FLAG-KAP1 N-ter RBCC{delta}mut dataset and 1 Input dataset done from HEK293 stable cells, 1 FLAG-KAP1 C-ter PB{delta}mut dataset and 1 Input dataset done from HEK293 stable cells. One FLAG-KAP1 N/C-ter (RBCC+PB){delta}mut dataset done from T-REx HEK293 stable cells. One endogenous KAP1 dataset done from HEK293 cells. Two independent ELK4 datasets done from duplicate HEK293 cells. One endogenous Kap1 dataset and one Input dataset from a stable cell line derived from U2OS cells.
2011-05-24 | E-GEOD-27929 | biostudies-arrayexpress
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2011-04-04 | E-GEOD-28286 | biostudies-arrayexpress
Project description:Cbx3 (HP1γ) that is a member of the heterochromatin protein 1 familiy enriched in gene bodies of pluripotent ESCs but promoters of differentiated pre-iPSCs. To determine whether Cbx3 becomes enriched at promoters to influence gene regulation during differentiation, we converted ESCs to NPCs in monolayer culuture and performed genomewide ChIP-seq of Cbx3. Our results shows that Cbx3 enriches at the promoters of genes upon differentiation of ESCs to NPCs and stablizes the binding of Mediator subunit Med26 to pre-initiation complex (PIC) in NPCs.
2017-03-27 | GSE89573 | GEO
Project description:Human MBT domain-containing protein L3MBTL2 was found to be an integral component of a protein complex that we termed Polycomb Repressive Complex 1-like 3 (PRC1L3) given the presence of the PcG proteins RING1, RING2 and PCGF6. L3MBTL2 binds chromatin in a histone modification-independent manner and is required for the repressive function of PRC1L3. PRC1L3 also contains E2F6 and CBX3, two factors with wellM-bM-^@M-^Pestablished functions in transcriptional repression. GenomeM-bM-^@M-^Pwide profiling identified several hundred genes that are simultaneously bound by L3MBTL2 and E2F6, preferentially around transcriptional start sites. Importantly, these genes are largely distinct from those targeted by other E2Fs or L3MBTL, another MBTM-bM-^@M-^Pdomain containing protein that interacts with RB1. H3K27 or H3K9 methylation, two chromatin modifications implicated in gene silencing, are not present on all L3MBTL2 target genes. L3MBTL2-specific RNAi results in altered target gene expression patterns and affects the differentiation program of hematopoietic cells. Our data suggest that repression of transcription via chromatin modulation, reflective of PRC1 function, can be achieved by multiple players and does not necessarily require the presence of histone lysine methylation marks. 7 total ChIP-seq datasets; one L3MBTL2 dataset done in duplicate in K562 cells; one E2F6 dataset done in duplicate in K562 cells; one H3K27me3 replicate dataset in K562 cells.
2011-06-07 | E-GEOD-28162 | biostudies-arrayexpress