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Mitotic chromosome binding predicts transcription factor properties in interphase [ChIP-Seq]

ABSTRACT: Mitotic chromosome binding predicts transcription factor properties in interphase [ChIP-Seq]

PROVIDER: PRJNA490289 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7817880_1.fastq.gz	Fastqsanger.gz
	SRR7817880_2.fastq.gz	Fastqsanger.gz
	SRR7817890_1.fastq.gz	Fastqsanger.gz
	SRR7817890_2.fastq.gz	Fastqsanger.gz
	SRR7817900_1.fastq.gz	Fastqsanger.gz

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Mitotic chromosome binding predicts transcription factor properties in interphase

Project description:Mitotic chromosome binding predicts transcription factor properties in interphase

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Mitotic chromosome binding predicts transcription factor properties in interphase [ATAC-Seq]

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Mitotic chromosome binding predicts transcription factor properties in interphase [ATAC-Seq]

Project description:Mammalian transcription factors (TFs) differ broadly in their nuclear mobility and sequence-specific/ non-specific DNA binding affinity. How these properties affect the ability of TFs to occupy their specific binding sites in the genome and modify the epigenetic landscape is unclear. Here we combined live cell quantitative measurements of mitotic chromosome binding (MCB) of 502 TFs, measurements of TF mobility by fluorescence recovery after photobleaching, single molecule imaging of DNA binding in live cells, and genome-wide mapping of TF binding and chromatin accessibility. MCB scaled with interphase properties such as association with DNA-rich compartments, mobility, as well as large differences in genome-wide specific site occupancy that correlated with TF impact on chromatin accessibility. As MCB is largely mediated by electrostatic, non-specific TF-DNA interactions, our data suggests that non-specific DNA binding of TFs enhances their search for specific sites and thereby their impact on the accessible chromatin landscape.

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Interphase chromosome conformation is specified by distinct folding programs inherited via mitotic chromosomes or through the cytoplasm [Hi-C]

Project description:Identity-specific interphase chromosome conformation must be re-established each time a cell divides. To understand how interphase folding is inherited, we developed an experimental approach that physically segregates mediators of G1 folding that are intrinsic to mitotic chromosomes from cytoplasmic factors. Proteins essential for nuclear transport, RanGAP1 and Nup93, were degraded in pro-metaphase arrested DLD-1 cells to prevent the establishment of nucleo-cytoplasmic transport during mitotic exit and isolate the decondensing mitotic chromatin of G1 daughter cells from the cytoplasm. Using this approach, we discover a transient folding intermediate entirely driven by chromosome-intrinsic factors. In addition to conventional compartmental segregation, the chromosome-intrinsic folding program leads to prominent genome-scale microcompartmentalization of mitotically bookmarked and cell type-specific cis-regulatory elements. The microcompartment conformation is formed during telophase and subsequently modulated by a second folding program driven by factors inherited through the cytoplasm in G1. This nuclear import-dependent folding program includes cohesin and factors involved in transcription and RNA processing. The combined and inter-dependent action of chromosome-intrinsic and cytoplasmic inherited folding programs determines the interphase chromatin conformation as cells exit mitosis.

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Interphase chromosome conformation is specified by distinct folding programs inherited via mitotic chromosomes or through the cytoplasm [ATAC-seq]

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Interphase chromosome conformation is specified by distinct folding programs inherited via mitotic chromosomes or through the cytoplasm [CUT&Run]

Project description:Identity-specific interphase chromosome conformation must be re-established each time a cell divides. To understand how interphase folding is inherited, we developed an experimental approach that segregates chromosome-intrinsic factors from those inherited through the cytoplasm during the establishment of G1 nuclear architecture. Endogenous RanGAP1 or Nup93 proteins were degraded in pro-metaphase arrested DLD-1 cells to prevent the establishment of nucleo-cytoplasmic transport during mitotic exit and isolate the decondensing mitotic chromatin of G1 daughter cells from the cytoplasm. Using this approach, we uncovered a transient folding intermediate entirely driven by chromosome-intrinsic factors. In addition to conventional compartmental segregation, this chromosome-intrinsic folding program leads to prominent genome-scale microcompartmentalization of mitotically bookmarked and cell type-specific cis-regulatory elements. The microcompartment conformation is formed during telophase and subsequently modulated by a second folding program driven by factors inherited through the cytoplasm in G1. The nuclear import-dependent folding program includes cohesin and factors involved in transcription and RNA processing. The combined and inter-dependent action of chromosome-intrinsic and cytoplasmic inherited folding programs determines the interphase chromatin conformation as cells exit mitosis.

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Interphase chromosome conformation is specified by distinct folding programs inherited via mitotic chromosomes or through the cytoplasm [SLAM-seq]

Project description:Identity-specific interphase chromosome conformation must be re-established each time a cell divides. To understand how interphase folding is inherited, we developed an experimental approach that segregates chromosome-intrinsic factors from those inherited through the cytoplasm during the establishment of G1 nuclear architecture. Endogenous RanGAP1 or Nup93 proteins were degraded in pro-metaphase arrested DLD-1 cells to prevent the establishment of nucleo-cytoplasmic transport during mitotic exit and isolate the decondensing mitotic chromatin of G1 daughter cells from the cytoplasm. Using this approach, we uncovered a transient folding intermediate entirely driven by chromosome-intrinsic factors. In addition to conventional compartmental segregation, this chromosome-intrinsic folding program leads to prominent genome-scale microcompartmentalization of mitotically bookmarked and cell type-specific cis-regulatory elements. The microcompartment conformation is formed during telophase and subsequently modulated by a second folding program driven by factors inherited through the cytoplasm in G1. The nuclear import-dependent folding program includes cohesin and factors involved in transcription and RNA processing. The combined and inter-dependent action of chromosome-intrinsic and cytoplasmic inherited folding programs determines the interphase chromatin conformation as cells exit mitosis.

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Mitotic chromosome binding predicts transcription factor properties in interphase.

Project description:Mammalian transcription factors (TFs) differ broadly in their nuclear mobility and sequence-specific/non-specific DNA binding. How these properties affect their ability to occupy specific genomic sites and modify the epigenetic landscape is unclear. The association of TFs with mitotic chromosomes observed by fluorescence microscopy is largely mediated by non-specific DNA interactions and differs broadly between TFs. Here we combine quantitative measurements of mitotic chromosome binding (MCB) of 501 TFs, TF mobility measurements by fluorescence recovery after photobleaching, single molecule imaging of DNA binding, and mapping of TF binding and chromatin accessibility. TFs associating to mitotic chromosomes are enriched in DNA-rich compartments in interphase and display slower mobility in interphase and mitosis. Remarkably, MCB correlates with relative TF on-rates and genome-wide specific site occupancy, but not with TF residence times. This suggests that non-specific DNA binding properties of TFs regulate their search efficiency and occupancy of specific genomic sites.

| S-EPMC6353955 | biostudies-literature

Mitotic chromosome binding predicts transcription factor properties in interphase

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-01-25 | GSE119784 | GEO