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Concurrent Mapping of Multiple Epigenetic Marks and Co-enrichment Using ACT2-seq

ABSTRACT: Concurrent Mapping of Multiple Epigenetic Marks and Co-enrichment Using ACT2-seq

PROVIDER: PRJNA742015 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14931009_1.fastq.gz	Fastqsanger.gz
	SRR14931009_2.fastq.gz	Fastqsanger.gz
	SRR14931010_1.fastq.gz	Fastqsanger.gz
	SRR14931010_2.fastq.gz	Fastqsanger.gz

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Concurrent Mapping of Multiple Epigenetic Marks and Co-enrichment Using ACT2-seq

Project description:Genome-wide profiling of epigenetic marks is a core technology in molecular genetics. Co-occupancy of different epigenetic marks or protein factors on chromatin is often inferred from their existence at the same genomic locations. However, this strategy does not provide direct evidence whether the epigenetic marks or protein factors occupy the same chromatin loci in the same cell due to the existence of cellular heterogeneity. To address this issue, we report a technique termed ACT2-seq that is capable of concurrently profiling multiple epigenetic marks in a single biological sample. While profiling simultaneously different epigenetic marks or protein factors genome-wide, ACT2 is capable of directly detecting co-occupancy of two different marks or factors on chromatin. This strategy provides direct evidence of co-localization without requiring complex single-molecule, single-cell, or magnetic bead-based approaches. We conclude that ACT2 presents an attractive option for epigenomic profiling due to its ease of use, potential for reducing sample and sequencing costs, and ability to profile co-occupancy of different epigenetic marks and protein factors on chromatin

2021-12-08 | GSE179047 | GEO

Concurrent mapping of multiple epigenetic marks and co-occupancy using ACT2-seq.

Project description:BackgroundGenome-wide profiling of epigenetic marks is a core technology in molecular genetics. Co-occupancy of different epigenetic marks or protein factors at the same genomic locations must often be inferred from multiple independently collected data sets. However, this strategy does not provide direct evidence of co-enrichment in the same cells due to the existence of cellular heterogeneity. To address this issue, we have developed a technique termed ACT2-seq that is capable of concurrently profiling multiple epigenetic marks in a single biological sample. In addition to reducing the numbers of samples required for experiments, ACT2-seq is capable of mapping co-occupancy of epigenetic factors on chromatin. This strategy provides direct evidence of co-enrichment without requiring complex single-molecule, single-cell, or magnetic bead-based approaches.ResultsWe concurrently profiled pairs of two epigenetic marks using ACT2-seq as well as three marks in individual samples. Data obtained using ACT2-seq were found to be reproducible and robust. ACT2-seq was capable of cleanly partitioning concurrently mapped data sets that exhibited distinct enrichment patterns. Using ACT2-seq, we identified distinct relationships between co-occupancy of specific histone modifications and gene expression patterns.ConclusionsWe conclude that ACT2-seq presents an attractive option for epigenomic profiling due to its ease of use, potential for reducing sample and sequencing costs, and ability to simultaneously profile co-occupancy of multiple histone marks and/or chromatin-associated proteins.

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Concurrent gliomas in patients with multiple sclerosis

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Concurrent gliomas in patients with multiple sclerosis

Project description:Background: Concurrent malignant brain tumors in patients with multiple sclerosis (MS) constitute a rare but paradigmatic phenomenon for studying neuroimmunological mechanisms from both molecular and clinical perspectives. Methods: A multicenter cohort of 26 patients diagnosed with both primary brain tumors and multiple sclerosis was studied for disease localization, tumor treatment-related MS activity, and molecular characteristics specific for diffuse glioma in MS patients. Results: MS neither predisposes nor protects from the development of gliomas. Patients with glioblastoma WHO grade 4 without isocitratdehydrogenase (IDH) mutations have a longstanding history of MS, whereas patients diagnosed with IDH-mutant astrocytoma WHO grade 2 receive multiple sclerosis diagnosis mostly at the same time or later. Concurrent MS is associated with a lesser extent of tumor resection and a worse prognosis in IDH-mutant glioma patients (PFS 32 vs. 64 months, p=0.0206). When assessing tumor-intrinsic differences no distinct subgroup-defining methylation pattern is identified in gliomas of MS patients compared to other glioma samples. However, differential methylation of immune-related genetic loci including human leukocyte antigen locus on 6p21 and interleukin locus on 5q31 is found in MS patients vs. matched non-MS patients. In line, inflammatory disease activity increases in 42% of multiple sclerosis patients after brain tumor radiotherapy suggesting a susceptibility of multiple sclerosis brain tissue to pro-inflammatory stimuli such as ionizing radiation. Conclusions: Concurrent low-grade gliomas should be considered in multiple sclerosis patients with slowly progressive, expansive T2/FLAIR lesions. Our findings of typically reduced extent of resection in MS patients and increased MS activity after radiation may inform future treatment decisions.

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