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A Cut/cohesin axis altersthe chromatin landscape to facilitate neuroblast death

ABSTRACT: A Cut/cohesin axis altersthe chromatin landscape to facilitate neuroblast death

PROVIDER: PRJNA514805 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8436121.fastq.gz	Fastqsanger.gz
	SRR8436122.fastq.gz	Fastqsanger.gz
	SRR8436123.fastq.gz	Fastqsanger.gz
	SRR8436124.fastq.gz	Fastqsanger.gz

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A Cut/cohesin axis altersthe chromatin landscape to facilitate neuroblast death

Project description:Cut regulates the programmed death of neural stem cells by altering cohesin levels and promoting a more open chromatin conformation to allow cell death gene expression.

2019-04-17 | GSE124998 | GEO

A Cut/cohesin axis alters the chromatin landscape to facilitate neuroblast death.

Project description:Precise control of cell death in the nervous system is essential for development. Spatial and temporal factors activate the death of Drosophila neural stem cells (neuroblasts) by controlling the transcription of multiple cell death genes through a shared enhancer. The activity of this enhancer is controlled by abdominal A and Notch, but additional inputs are needed for proper specificity. Here, we show that the Cut DNA binding protein is required for neuroblast death, regulating reaper and grim downstream of the shared enhancer and of abdominal A expression. The loss of cut accelerates the temporal progression of neuroblasts from a state of low overall levels of H3K27me3 to a higher H3K27me3 state. This is reflected in an increase in H3K27me3 modifications in the cell death gene locus in the CNS on Cut knockdown. We also show that cut regulates the expression of the cohesin subunit Stromalin. Stromalin and the cohesin regulatory subunit Nipped-B are required for neuroblast death, and knockdown of Stromalin increases H3K27me3 levels in neuroblasts. Thus, Cut and cohesin regulate apoptosis in the developing nervous system by altering the chromatin landscape.

| S-EPMC6526717 | biostudies-literature

Neuroblast-specific open chromatin allows the temporal transcription factor, Hunchback, to bind neuroblast-specific loci

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PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression[CUT&RUN]

Project description:PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression[CUT&RUN]

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Cohesin is a key determinant of interphase chromosome domain architecture (HiC)

Project description:To ensure proper gene regulation within constrained nuclear space, chromosomes facilitate access to transcribed regions, while compactly packaging all other information. Recent studies revealed that chromosomes are organized into megabase-scale domains that demarcate active and inactive genetic elements, suggesting that compartmentalization is important for genome function. Here we show that very specific long-range interactions are anchored by cohesin/CTCF sites, but not cohesin-only or CTCF-only sites, to form a hierarchy of chromosomal loops. These loops demarcate topological domains and form intricate internal structures within them. Post-mitotic nuclei deficient for functional cohesin exhibit global architectural changes associated with loss of cohesin/CTCF contacts and relaxation of topological domains. Transcriptional analysis shows that this cohesin-dependent perturbation of domain organization leads to widespread gene deregulation of both cohesin-bound and non-bound genes. Our data thereby support a role for cohesin in the global organization of domain structure and suggest that domains function to stabilize the transcriptional programs within them. Hi-C, ChIP-Seq and RNA-Seq experiments were conducted in mouse neural stem cells and mouse astrocytes

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Project description:Neuroblast-specific open chromatin allows the temporal transcription factor, Hunchback, to bind neuroblast-specific loci

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Cohesin is a key determinant of interphase chromosome domain architecture (ChIP-seq)

2013-12-11 | E-GEOD-48938 | biostudies-arrayexpress