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Confined Migration Induces Heterochromatin Formation and Alters Chromatin Accessibility

ABSTRACT: Confined Migration Induces Heterochromatin Formation and Alters Chromatin Accessibility

PROVIDER: PRJNA751211 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15312003_1.fastq.gz	Fastqsanger.gz
	SRR15312003_2.fastq.gz	Fastqsanger.gz
	SRR15312004_1.fastq.gz	Fastqsanger.gz
	SRR15312004_2.fastq.gz	Fastqsanger.gz
	SRR15312005_1.fastq.gz	Fastqsanger.gz

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Confined Migration Induces Heterochromatin Formation and Alters Chromatin Accessibility

Project description:We show that confined migration results in predominantly decreased chromatin accessibility, consistent with the increased heterochromatin marks staining. A small fraction of ATAC-seq peaks shows increased accessibility at gene promoters of diverse pathways, such as chromatin silencing, tumor invasion, and DNA damage response; whereas the majority shows decreased accessibility at intergenic regions near centromeres or telomeres, suggesting possible heterochromatin spreading.

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Confined migration induces heterochromatin formation and alters chromatin accessibility.

Project description:During migration, cells often squeeze through small constrictions, requiring extensive deformation. We hypothesized that nuclear deformation associated with such confined migration could alter chromatin organization and function. By studying cells migrating through microfluidic devices that mimic interstitial spaces in vivo, we found that confined migration results in increased H3K9me3 and H3K27me3 heterochromatin marks that persist for days. This "confined migration-induced heterochromatin" (CMiH) was distinct from heterochromatin formation during migration initiation. Confined migration decreased chromatin accessibility at intergenic regions near centromeres and telomeres, suggesting heterochromatin spreading from existing sites. Consistent with the overall decrease in accessibility, global transcription was decreased during confined migration. Intriguingly, we also identified increased accessibility at promoter regions of genes linked to chromatin silencing, tumor invasion, and DNA damage response. Inhibiting CMiH reduced migration speed, suggesting that CMiH promotes confined migration. Together, our findings indicate that confined migration induces chromatin changes that regulate cell migration and other functions.

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RNA sequencing to analyze trasncriptional profiles and screen potential regulators in confined migration

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Project description:Heterochromatin is a specialized form of chromatin that restricts access to DNA and inhibits genetic processes, including transcription and recombination. In Neurospora crassa, constitutive heterochromatin is characterized by trimethylation of lysine 9 on histone H3, hypoacetylation of histones, and DNA methylation. Here we explore whether the conserved histone demethylase, lysine-specific demethylase 1 (LSD1), regulates heterochromatin in Neurospora, and if so, how. Though LSD1 is implicated in heterochromatin regulation, its function is inconsistent across different systems; orthologs of LSD1 have been shown to either promote or antagonize heterochromatin expansion by removing H3K4me or H3K9me respectively. We identify three members of the Neurospora LSD complex (LSDC): LSD1, PHF1, and BDP-1, and strains deficient for any exhibit variable spreading of heterochromatin and establishment of new heterochromatin domains dispersed across the genome. Heterochromatin establishment outside of canonical domains in Neurospora share the unusual characteristic of DNA methylation-dependent H3K9me3; typically, H3K9me3 establishment is independent of DNA methylation. Consistent with this, the hyper-H3K9me3 phenotype of LSD1 knock-out strains is dependent on the presence of DNA methylation, as well as HCHC-mediated histone deacetylation, suggesting spreading is dependent on some feedback mechanism. Altogether, our results suggest LSD1 works in opposition to HCHC to maintain proper heterochromatin boundaries.

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