Nucleosome-mediated competition of pioneer transcription factors
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PROVIDER: PRJNA891341 | ENA |
REPOSITORIES: ENA
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Project description:Pioneer transcription factors Nanog, Pou5f3 and Sox19b promote chromatin accessibility on the enhancers of the early zebrafish embryos. It is poorly understood how they act together; it is commonly assumed that they act additively or cooperatively to clear chromatin from the nucleosomes. We investigated this question by comparing chromatin accessibility (Omni ATAC-seq) in seven mutant genotypes: single, double and triple maternal-zygotic mutants by Pou5f3, Sox19b and Nanog, and the wild-type embryos. We found, that at most of the directly bound sites, either Pou or Nanog is required for chromatin accessibility; while at the minority of the sites two factors act additively. Further, on the sites, where Pou5f3 promotes chromatin accessibility, Nanog often suppresses it, and vice versa. To explain this phenomenon, we suggest a model of nucleosome-mediated competition between pioneer transcription factors: Pou5f3 and Nanog compete for the same binding motif on the DNA, but only one of the factors has a pioneer activity on this site. This entry contains only part fo the Omni-ATAC-seq experiments, the other part is in the previously released entry GSE188364.
2023-08-02 | GSE215956 | GEO
Project description:The nucleosome is a fundamental unit of chromatin in eukaryotes, and generally prevents the binding of transcription factors to genomic DNA. Pioneer transcription factors overcome the nucleosome barrier, and bind their target DNA sequences in chromatin. OCT4 is a representative pioneer transcription factor that plays a role in stem cell pluripotency. In the present study, we biochemically analyzed the nucleosome binding by OCT4. Crosslinking mass spectrometry showed that OCT4 binds the nucleosome.
2020-05-13 | PXD019160 | JPOST Repository
Project description:Purpose: The dynamic nucleosome reorganization is the interplay among nucleosome and regulated by pioneer factors, which can access target DNA sequences on nucleosomes.The goals of this study are revealing the dynamic nucleosome footprint and how GATA2 is capable of resetting crowding array to primed, or accessible edge nucleosome states. Methods: LNCaP cells between passage number 30-35 were used for assay. cell nucleus was extracted, digested by MNase to Mono-nucleosome and ChIP/ChIP-exo was performed, the ChIP products were further used to generate library with illumina ChIP-seq kit. Hi-seq 3000 was used for sequencing and the data was analyzed by MACS2 for peaks. Results: GATA2 is associated with condensed nucleosome states and nucleosomes could unwrapped and be more accessible in pioneer factor GATA2 binding sites. Conclusions: Our study represents the first detailed nucleosome footprint of LNCap cells and analysis of the relationship between pioneer factor GATA2 and nucleosome reorganization in whole genomic DNA. These results demonstrated GATA2 play a critical role in an AR-independent manner in prostate cancer.
2021-04-14 | GSE148935 | GEO
Project description:Summary: Pioneer transcription factors engage nucleosomal DNA in chromatin to initiate gene regulatory events that control cell fate 1 . To determine how different pioneer transcription factors initiate the formation of a locally accessible environment within silent, compacted chromatin and collaborate with an ATP-dependent chromatin remodeler, we generated nucleosome arrays in vitro with a central nucleosome that can be targeted by the hematopoietic ETS factor PU.1 and bZIP factors C/EBPα, and C/EBPβ. Each class of factor can expose target nucleosomes on linker histone-compacted arrays, but with different hypersensitivity patterns, as discerned by long-read sequencing. The DNA binding domain of PU.1 is sufficient for mononucleosome binding but requires an additional intrinsically disordered domain to bind and open compacted chromatin. The canonical mammalian SWI/SNF (BAF) complex, cBAF, was unable to act upon two forms of locally open chromatin, in the presence of linker histone, unless cBAF was enabled by the acidic- and glutamine-enriched transactivation domain of PU.1. However, cBAF complexes potentiate the nucleosome binding DBD of PU.1 to weakly open chromatin in the absence of the PU.1 unstructured domain. Together our findings provide a mechanism for how pioneer factors initially target chromatin structures to provide specificity for action by nucleosome remodelers that further open local domains.
2022-11-03 | GSE216065 | GEO
Project description:Though the in vitro structural and in vivo spatial characteristics of transcription factor (TF) binding are well defined, TF interactions with chromatin and other companion TFs during development are poorly understood. To analyze such interactions in vivo, we profiled several TFs across a time course of human embryonic stem cell differentiation via CUT&RUN epigenome profiling, and studied their interactions with nucleosomes and co-occurring TFs by Enhanced Chromatin Occupancy (EChO), a computational strategy for classifying TF binding characteristics across time and space. EChO shows that at different enhancer targets, the same TF can employ either direct DNA binding, or “pioneer” nucleosome binding to access them. Pioneer binding is correlated with local binding of other TFs and enhancer motif character, including degeneracy at key bases in the pioneer factor target motif. Our strategy reveals a dynamic exchange of TFs at enhancers across developmental time that is aided by pioneer nucleosome binding.
2019-06-25 | GSE128499 | GEO
Project description:When stem cells activate a member of the SOX family of pioneer factors, they bind their cognate sequences within condensed chromatin, not only evicting the associated nucleosome, but also recruiting H3K4-monomethylases, which modify flanking nucleosomes to open chromatin and activate one lineage program; simultaneously, pioneer factors also silence alternative fates, but in this case act indirectly, through competing for H3K4-monomethylases pre-existing at the original fate genes.
2023-05-05 | GSE208071 | GEO
Project description:When stem cells activate a member of the SOX family of pioneer factors, they bind their cognate sequences within condensed chromatin, not only evicting the associated nucleosome, but also recruiting H3K4-monomethylases, which modify flanking nucleosomes to open chromatin and activate one lineage program; simultaneously, pioneer factors also silence alternative fates, but in this case act indirectly, through competing for H3K4-monomethylases pre-existing at the original fate genes.
2023-05-05 | GSE208070 | GEO
Project description:When stem cells activate a member of the SOX family of pioneer factors, they bind their cognate sequences within condensed chromatin, not only evicting the associated nucleosome, but also recruiting H3K4-monomethylases, which modify flanking nucleosomes to open chromatin and activate one lineage program; simultaneously, pioneer factors also silence alternative fates, but in this case act indirectly, through competing for H3K4-monomethylases pre-existing at the original fate genes.
2023-05-05 | GSE208066 | GEO
Project description:When stem cells activate a member of the SOX family of pioneer factors, they bind their cognate sequences within condensed chromatin, not only evicting the associated nucleosome, but also recruiting H3K4-monomethylases, which modify flanking nucleosomes to open chromatin and activate one lineage program; simultaneously, pioneer factors also silence alternative fates, but in this case act indirectly, through competing for H3K4-monomethylases pre-existing at the original fate genes.
2023-05-05 | GSE208069 | GEO
Project description:Nucleosome-displacing factors (NDFs) in yeast, similar to pioneer factors in higher eukaryotes, cause opening of closed chromatin and formation of nucleosome-depleted regions (NDRs). NDRs in yeast are also affected by ATP-dependent chromatin remodelers (CRs). However, how NDFs and CRs coordinate in nucleosome invasion and NDR formation is still unclear. Here, we designed a high-throughput method to systematically study the interplay between NDFs and CRs. By combining integrated synthetic oligonucleotide library with DNA methyltransferase-based, single-molecule nucleosome mapping, we measured the impact of CRs on NDRs generated by individual NDFs. We found that CRs were dispensable for nucleosome invasion by NDFs, and they function downstream of NDF binding to modulate the NDR length. A few CRs show high specificity towards certain NDFs; however, in most cases, CRs are recruited in a factor-nonspecific and length-dependent manner. Overall, our study represents a novel framework to investigate how NDFs and CRs cooperate to generate desired pattern of chromatin opening.
2022-04-06 | GSE199812 | GEO