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Somatic mutation distributions in cancer genomes vary with three-dimensional chromatin structure

ABSTRACT: Somatic mutation distributions in cancer genomes vary with three-dimensional chromatin structure

PROVIDER: PRJNA491824 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7875950_1.fastq.gz	Fastqsanger.gz
	SRR7875950_2.fastq.gz	Fastqsanger.gz
	SRR7875951_1.fastq.gz	Fastqsanger.gz
	SRR7875951_2.fastq.gz	Fastqsanger.gz
	SRR7875952_1.fastq.gz	Fastqsanger.gz

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Somatic mutation distributions in cancer genomes vary with three-dimensional chromatin structure

Project description:Somatic mutations arise during the life history of a cell. Mutations occurring in cancer driver genes may ultimately lead to the development of clinically detectable disease. Nascent cancer lineages continue to acquire somatic mutations throughout the neoplastic process and during cancer evolution. Extrinsic and endogenous mutagenic factors contribute to the accumulation of these somatic mutations. Understanding the underlying causes of mutations is critical for developing potential preventions and tailoring the clinical treatments. Earlier studies have revealed that DNA replication timing and chromatin modifications are associated with variations in mutational density. In order to understand the interplay between spatial genome organization and individual mutational processes, we report here a study of more than 3000 whole genome datasets from 50 different cancer studies. Our analyses revealed that different mutational processes lead to distinct somatic mutation distributions between chromatin folding domains. APOBEC- or MSI-related mutations are enriched in transcriptionally-active domains while mutations occurring due to tobacco-smoke and ultraviolet (UV) light exposure or a gastric flux-related mutational signature (signature 17) enrich predominantly in transcriptionally-inactive domains. Active mutational processes dictate the mutation distributions in cancer genomes, therefore mutational distributions could shift during cancer evolution upon mutational processes switch. Moreover, a dramatic instance of extreme chromatin structure in humans, that of the unique folding pattern of the inactive X-chromosome leads to distinct somatic mutation distribution on X chromosome in females compared to males in various cancer types. Overall, the interplay between three-dimensional genome organization and active mutational processes has a substantial influence on the large-scale mutation rate variations observed in human cancer.

2020-07-01 | GSE120166 | GEO

Somatic mutation distributions in cancer genomes vary with three-dimensional chromatin structure.

Project description:Somatic mutations in driver genes may ultimately lead to the development of cancer. Understanding how somatic mutations accumulate in cancer genomes and the underlying factors that generate somatic mutations is therefore crucial for developing novel therapeutic strategies. To understand the interplay between spatial genome organization and specific mutational processes, we studied 3,000 tumor-normal-pair whole-genome datasets from 42 different human cancer types. Our analyses reveal that the change in somatic mutational load in cancer genomes is co-localized with topologically-associating-domain boundaries. Domain boundaries constitute a better proxy to track mutational load change than replication timing measurements. We show that different mutational processes lead to distinct somatic mutation distributions where certain processes generate mutations in active domains, and others generate mutations in inactive domains. Overall, the interplay between three-dimensional genome organization and active mutational processes has a substantial influence on the large-scale mutation-rate variations observed in human cancers.

| S-EPMC8350746 | biostudies-literature

Three-dimensional molecular architecture of mouse organogenesis

Project description:Mammalian embryos exhibits sophisticated cell organizations that are intricately orchestrated at both molecular and cellular level. It has recently become apparent that cells within the animal body display significant heterogeneity, both in terms of their cellular properties and their spatial distributions. However, current spatial transcriptomics profiling either lack three-dimensional representation or are limited in their ability to capture the complexity of embryonic tissues and organs. Here, we present a represented spatial transcriptome atlas of all major organs at embryonic day 13.5 (E13.5) in the mouse embryo, and provide a three- dimensional rendering of molecular regulation for embryonic patterning with stacked sections. By integrating this spatial transcriptome data with corresponding single-cell transcriptome data, we offer a detailed molecular annotation of the dynamic nature of organ development, spatial cellular interaction, embryonic axes and divergence of cell fates underlying mammalian development, which would pave the way for precise organ engineering and stem cell-based regenerative medicine.

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Phase 0 study of three-dimensional endoscopic optical coherence tomography (u-VOIS)

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Project description:Colorectal cancer (CRC) shows the high mortality and morbidity. The mortal number of patients and the morbid number of patients with CRC is also increasing. However, the genes which relate to promote tumorigenesis in CRC remain unclear. In order to investigate specific genes and pathways involved in CRC tumorigenesis, we compared genes expressed between three dimensional cultures and control two-dimensional cultures. Total RNA was prepared from the CRC cell lines under the condition of two-dimensional culture and three dimensional culture.

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2024-03-07 | GSE254976 | GEO

Three-dimensional molecular architecture of mouse organogenesis

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TFIIIC and MYCN link the three-dimensional chromatin structure of promoters to transcription termination of stalled RNA polymerase (ChIPseq CnR)

Project description:MYC proteins bind to virtually all active promoters transcribed by RNA polymerase II (RNAPII), but whether they interact with the three-dimensional chromatin architecture is unknown. Here we used HiChIP sequencing of the MYCN oncoprotein and found that MYCN localizes to three-dimensional hubs formed by active promoters and enhancers. In these hubs, MYCN interacts with TFIIIC, an architectural protein complex. MYCN recruits TFIIIC to promoters when transcription elongation is inhibited, and the complex of both proteins induces premature transcription termination. Termination correlates closely with the TFIIIC-dependent removal of MYCN from promoter hubs and with corresponding alterations in the three-dimensional interactions of cohesin complexes. This limits DNA damage by removing RNAPII that stalls proximal to double-strand breaks. Binding of TFIIIC to MYCN is limited by competition with Aurora-A and this protects genes involved in mRNA processing from termination, arguing that MYCN contributes to the unusual proliferative capacity of neuroblastoma cells via removing stalled RNAPII from promoter hubs and via increasing the capacity for RNA processing.

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