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Dynamic genome-wide interaction patterns elucidate the roles of Ki67 in chromatin organization

ABSTRACT: Dynamic genome-wide interaction patterns elucidate the roles of Ki67 in chromatin organization

PROVIDER: PRJNA772958 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16497400.fastq.gz	Fastqsanger.gz
	SRR16497500.fastq.gz	Fastqsanger.gz
	SRR16497600.fastq.gz	Fastqsanger.gz
	SRR16497401.fastq.gz	Fastqsanger.gz
	SRR16497501.fastq.gz	Fastqsanger.gz

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Dynamic genome-wide interaction patterns elucidate the roles of Ki67 in chromatin organization

Project description:Ki67 is a widely-used proliferation marker with functions in chromosomal organization. It forms a protective layer around mitotic chromosomes and is involved in genome positioning in interphase. However, a detailed understanding of how Ki67 organizes the genome was still lacking, partially because genome-wide interaction profiles were missing. Here, we generate DNA-Ki67 interaction profiles using our pA-DamID method, and show that Ki67 interacts with the genome in a domain-like pattern that partially overlaps with lamina-associated domains.

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Ki67-mediated chromatin accessibility impedes B-cell antigen-receptor gene rearrangement

Project description:B and T cells can recognise and respond to a vast array of foreign pathogens by virtue of the diverse antigen-receptor repertoire generated by gene rearrangement during development. Here, we show that deficiency in Ki67, a nuclear protein ubiquitously expressed throughout the cell cycle, impairs B-cell development at specific, early stages. We identified that Ki67 maintains global chromatin accessibility in lymphocyte progenitors at stages where antigen-receptor gene rearrangements occur and that gene rearrangement is less efficient in the absence of Ki67. That the defects in B cell development are caused by disrupted antigen-receptor gene rearrangement is shown by pre-rearranged antigen-receptor genes fully compensating for loss of Ki67. Collectively, these results identify a unique contribution from Ki67 to somatic antigen-receptor gene rearrangement.

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Project description:Lineage-specific gene expression is modulated by a balance between transcriptional activation and repression during animal development. Knowledge about enhancer-centered transcriptional activation has advanced considerably, but silencers and their roles in normal development remain poorly understood. Here, we performed chromatin interaction analyses of Polycomb repressive complex 2 (PRC2), a key inducer of transcriptional gene silencing, to uncover silencers, their molecular identity and associated chromatin connectivity. Systematic analysis of cis-regulatory silencer elements reveals their chromatin features and gene-targeting specificity. Deletion of certain PRC2-bound silencers in mice results in transcriptional derepression of their interacting genes and pleiotropic developmental phenotypes, including embryonic lethality. While some PRC2-bound elements function as silencers in pluripotent cells, they can transition into active tissue-specific enhancers during development, highlighting their regulatory versatility. Our study characterizes the molecular profile of silencers and their associated chromatin architectures, and suggests the possibility of targeted reactivation of epigenetically silenced genes.

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