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Competition shapes the landscape of X-linked genetic diversity [ChIP-seq]

ABSTRACT: Competition shapes the landscape of X-linked genetic diversity [ChIP-seq]

PROVIDER: PRJNA1088129 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28348497.fastq.gz	Fastqsanger.gz
	SRR28348498.fastq.gz	Fastqsanger.gz

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Competition shapes the landscape of X-linked genetic diversity

Project description:Competition shapes the landscape of X-linked genetic diversity

| PRJNA1088124 | ENA

Competition shapes the landscape of X-linked genetic diversity [scRNA-seq]

Project description:Competition shapes the landscape of X-linked genetic diversity [scRNA-seq]

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Competition shapes the landscape of X-linked genetic diversity [ChIP-seq]

Project description:Human populations harbour sequence variants even within essential genes. As a result of random X chromosome inactivation (XCI) and epigenetically stable XCI propagation, X-linked variation gives rise to genetically diverse clones that co-exist within XX individuals. Whether interactions between such clones shape the deployment of X-linked diversity remains to be explored. To address this question, we focus on benign coding variation in the X-linked STAG2 gene. Mouse models reveal that clones expressing Stag2 variants contribute to tissues such as skin and brain at the expected frequencies, but show reduced contributions to the haematopoietic stem and progenitor cell pool, and severely defective lymphoid specification. Unexpectedly, the absence of Xvariant clones from the lymphoid compartment is due not to cell-intrinsic defects, but requires competitive interactions with Xwt clones: in the absence of Xwt, Xvariant cells generate normal numbers of functional lymphocytes. X-linked competition has hallmarks of non-cell-autonomous 'cell competition', known to operate in a range of biological processes including embryonic development, aging, and cancer. These findings show that interactions between genetically diverse clones that may operate in any XX individual can shape the contribution of X-linked diversity to specific cell types and tissues.

2024-07-17 | GSE261621 | GEO

Competition shapes the landscape of X-linked genetic diversity [scRNA-seq]

2024-07-17 | GSE240997 | GEO

Competition shapes the landscape of X-chromosome-linked genetic diversity.

Project description:X chromosome inactivation (XCI) generates clonal heterogeneity within XX individuals. Combined with sequence variation between human X chromosomes, XCI gives rise to intra-individual clonal diversity, whereby two sets of clones express mutually exclusive sequence variants present on one or the other X chromosome. Here we ask whether such clones merely co-exist or potentially interact with each other to modulate the contribution of X-linked diversity to organismal development. Focusing on X-linked coding variation in the human STAG2 gene, we show that Stag2variant clones contribute to most tissues at the expected frequencies but fail to form lymphocytes in Stag2WT Stag2variant mouse models. Unexpectedly, the absence of Stag2variant clones from the lymphoid compartment is due not solely to cell-intrinsic defects but requires continuous competition by Stag2WT clones. These findings show that interactions between epigenetically diverse clones can operate in an XX individual to shape the contribution of X-linked genetic diversity in a cell-type-specific manner.

| S-EPMC11319201 | biostudies-literature

Competition shapes the landscape of X-linked genetic diversity

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

2024-07-17 | GSE261622 | GEO

The competition between splicing and 3′ processing shapes the human transcriptome

Project description:The competition between splicing and 3′ processing shapes the human transcriptome

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DNA methylation shapes the Polycomb landscape during the exit from naive pluripotency

Project description:To formally assess how 5mC shapes the H3K27me3 landscape, we profiled the epigenome of naive and differentiated cells in the presence and absence of the DNA methylation machinery.

2024-07-16 | GSE242201 | GEO

Protein expression signature in cell competition in HCC

Project description:Although increasing studies have proved cell competition widely involved in the growth and homeostasis of multicellular organisms is closely linked to tumorigenesis and development, the mechanistic contributions between drug resistance and tumor cell competition remain ill-defined. In this paper, we applied MS of cell competition group to determine the dominant characteristics of lenvatinib resistance and its metabolic differences in cell competition. Our results showed a vital role of HSP90-IDH1 mediated lipid accumulation in maintaining the competitive outcome of HCC drug-resistant cells via regulating lipid metabolism. HSP90-IDH1 axis could be a promising target to overcome HCC drug resistance.

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Spatial competition shapes the dynamic mutational landscape of normal esophageal epithelium.

Project description:During aging, progenitor cells acquire mutations, which may generate clones that colonize the surrounding tissue. By middle age, normal human tissues, including the esophageal epithelium (EE), become a patchwork of mutant clones. Despite their relevance for understanding aging and cancer, the processes that underpin mutational selection in normal tissues remain poorly understood. Here, we investigated this issue in the esophageal epithelium of mutagen-treated mice. Deep sequencing identified numerous mutant clones with multiple genes under positive selection, including Notch1, Notch2 and Trp53, which are also selected in human esophageal epithelium. Transgenic lineage tracing revealed strong clonal competition that evolved over time. Clone dynamics were consistent with a simple model in which the proliferative advantage conferred by positively selected mutations depends on the nature of the neighboring cells. When clones with similar competitive fitness collide, mutant cell fate reverts towards homeostasis, a constraint that explains how selection operates in normal-appearing epithelium.

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