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Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration [BLISS]

ABSTRACT: Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration [BLISS]

PROVIDER: PRJNA945055 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23873700.fastq.gz	Fastqsanger.gz
	SRR23873701.fastq.gz	Fastqsanger.gz
	SRR23873702.fastq.gz	Fastqsanger.gz
	SRR23873703.fastq.gz	Fastqsanger.gz
	SRR23873704.fastq.gz	Fastqsanger.gz

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Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration [BLISS]

Project description:Persistent DNA double-strand breaks (DSBs) in neurons are an early pathological hallmark of neurodegenerative diseases including Alzheimer’s Disease (AD), with the potential to disrupt genome integrity. We used single-nucleus RNA-seq in human post-mortem prefrontal cortex samples and found that excitatory neurons in AD were enriched for somatic mosaic gene fusions. Gene fusions were particularly enriched in excitatory neurons with DNA damage repair and senescence gene signatures. In addition, somatic genome structural variations and gene fusions were enriched in neurons burdened with DSBs in the CK-p25 mouse model of neurodegeneration. Neurons enriched for DSBs also had elevated levels of cohesin along with progressive multiscale disruption of the 3D genome organization aligned with transcriptional changes in synaptic, neuronal development, and histone genes. Overall, this study demonstrates the disruption of genome stability and the 3D genome organization by DSBs in neurons as pathological steps in the progression of neurodegenerative diseases.

2023-09-27 | GSE227438 | GEO

Nucleosomes protect DNA from irradiation-induced double strand breaks in living cells [BLISS human]

Project description:The number and position of breaks using BLISS-seq was measured in MCF-7 cells upon irradiation with 10 Gy and with or without the use of the antioxidant (N-acetylcysteine, NAC, 10mM).

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Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration [Mate-Pair]

Project description:Persistent DNA double-strand breaks (DSBs) in neurons are an early pathological hallmark of neurodegenerative diseases including Alzheimer’s Disease (AD) with the potential to disrupt genome integrity. We show increased mosaic structural variations and gene fusions in neurons burdened with DSBs in the CK-p25 inducible mouse model of neurodegeneration. Next, we used full-transcript single-nucleus RNA-seq across 47 human post-mortem prefrontal cortex and find that excitatory neurons in AD are enriched for mosaic gene fusions. In addition, gene fusions are particularly enriched in excitatory neurons with senescence and DNA repair gene signatures. Neurons enriched for DSBs also have elevated levels of cohesin along with progressive multiscale disruption of the 3D genome organization aligned with transcriptional changes in synaptic and neuronal development genes. Overall, this study demonstrates the disruption of genome stability and the 3D genome organization by DSBs in neurons as pathological steps in the progression of neurodegenerative diseases.

2023-09-27 | GSE227444 | GEO

Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration [Hi-C]

2023-09-27 | GSE227443 | GEO

Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration

Project description:Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration

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Genome-wide detection of DNA double-strand breaks by in-suspension BLISS

Project description:sBLISS (in-suspension Break Labeling In Situ and Sequencing) is a versatile and widely applicable method for identification of endogenous and induced DNA double-strand breaks (DSBs), in any cell type that can be brought into suspension. After in situ labeling, DSB ends are linearly amplified followed by next-generation sequencing and DSB landscape analysis. Here, we present a step-by-step experimental protocol for sBLISS, followed by a basic computational analysis. The main advantages of sBLISS are (i) the suspension setup, which circumvents the need to work with delicate coverslips as in the original BLISS, (ii) the possibility for adaptation to a high-throughput robotics or single-cell workflow, and (iii) its flexibility and applicability to virtually every cell type, including patient-derived cells, organoids, and isolated nuclei. The wet-lab protocol can be completed in 1.5 weeks, and it is suitable for researchers with intermediate expertise in molecular biology and genomics. For the computational analyses, basic-to-intermediate bioinformatics expertise is required.

2020-09-30 | GSE145598 | GEO

Nucleosomes protect DNA from irradiation-induced double strand breaks in living cells (BLISS)

Project description:The depletion of HMGB1 reduces the deposition of histones on naked DNA (Celona et al, 2011). in primary MEFs and yeast. We verified that the downmodulation of HMGB1 decreases histone level also in a model of murine mesothelioma. HMGB1 was KD in Murine Mesothelioma AB22 cells by the expression of a shRNA. Nucleosome positioning and occupancy were tested by ATAC-seq. Since a reduced amount of nucleosomes increase the cell sensitivity to gamma irradiatio, we tested the number and position of breaks using BLISS-seq.

2020-07-07 | GSE134797 | GEO

Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration.

Project description:Persistent DNA double-strand breaks (DSBs) in neurons are an early pathological hallmark of neurodegenerative diseases including Alzheimer's disease (AD), with the potential to disrupt genome integrity. We used single-nucleus RNA-seq in human postmortem prefrontal cortex samples and found that excitatory neurons in AD were enriched for somatic mosaic gene fusions. Gene fusions were particularly enriched in excitatory neurons with DNA damage repair and senescence gene signatures. In addition, somatic genome structural variations and gene fusions were enriched in neurons burdened with DSBs in the CK-p25 mouse model of neurodegeneration. Neurons enriched for DSBs also had elevated levels of cohesin along with progressive multiscale disruption of the 3D genome organization aligned with transcriptional changes in synaptic, neuronal development, and histone genes. Overall, this study demonstrates the disruption of genome stability and the 3D genome organization by DSBs in neurons as pathological steps in the progression of neurodegenerative diseases.

| S-EPMC10697236 | biostudies-literature

Genome-wide detection of DNA double-strand breaks by in-suspension BLISS

Project description:Genome-wide detection of DNA double-strand breaks by in-suspension BLISS

| PRJNA607701 | ENA

Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration [Mate-Pair]

Project description:Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration [Mate-Pair]

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