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Distinguishing between recruitment and spread of silent chromatin structures in Saccharomyces cerevisiae [I]

ABSTRACT: Distinguishing between recruitment and spread of silent chromatin structures in Saccharomyces cerevisiae [I]

PROVIDER: PRJNA781240 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16967349_1.fastq.gz	Fastqsanger.gz
	SRR16967349_2.fastq.gz	Fastqsanger.gz
	SRR16967350_1.fastq.gz	Fastqsanger.gz
	SRR16967350_2.fastq.gz	Fastqsanger.gz
	SRR16967351_1.fastq.gz	Fastqsanger.gz

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Distinguishing between recruitment and spread of silent chromatin structures in Saccharomyces cerevisiae

Project description:Distinguishing between recruitment and spread of silent chromatin structures in Saccharomyces cerevisiae

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Distinguishing between recruitment and spread of silent chromatin structures in Saccharomyces cerevisiae [II]

Project description:Distinguishing between recruitment and spread of silent chromatin structures in Saccharomyces cerevisiae [II]

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Distinguishing between recruitment and spread of silent chromatin structures in Saccharomyces cerevisiae [I]

Project description:The formation of heterochromatin at HML, HMR, and telomeres in Saccharomyces cerevisiae involves two main steps: Recruitment of Sir proteins to silencers and their spread throughout the silenced domain. For the following datasets, we created a fusion protein between the heterochromatin protein Sir3 and the non-site-specific bacterial adenine methyltransferase M.EcoGII, with or without a 3xV5 epitope at the C-terminus. We performed ChIP-seq experiments (immunoprecipitated Sir3-M.EcoGII-3xV5) and MeDIP-seq experiments (immunoprecipitated m6A methylated DNA). We also used a temperature-sensitive allele of SIR3 (sir3-8) fused to M.ECOGII to induce m6A methylation for MeDIP-seq.

2021-11-24 | GSE189038 | GEO

Distinguishing between recruitment and spread of silent chromatin structures in Saccharomyces cerevisiae [II]

Project description:The formation of heterochromatin at HML, HMR, and telomeres in Saccharomyces cerevisiae involves two main steps: Recruitment of Sir proteins to silencers and their spread throughout the silenced domain. For the following datasets, we created a fusion protein between the heterochromatin protein Sir3 and the non-site-specific bacterial adenine methyltransferase M.EcoGII. We mapped sites of Sir3-chromatin interactions genome-wide using long-read Nanopore sequencing to detect adenines methylated by the fusion protein. We also used a temperature-sensitive allele of SIR3 (sir3-8) fused to M.ECOGII to induce m6A methylation over time. Time courses involved a switch from restrictive temperature (37°C) to permissive temperature (25°C).

2022-01-17 | GSE190136 | GEO

Distinguishing between recruitment and spread of silent chromatin structures in Saccharomyces cerevisiae

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

2021-12-03 | GSE190137 | GEO

Distinguishing between recruitment and spread of silent chromatin structures in Saccharomyces cerevisiae.

Project description:The formation of heterochromatin at HML, HMR, and telomeres in Saccharomyces cerevisiae involves two main steps: the recruitment of Sir proteins to silencers and their spread throughout the silenced domain. We developed a method to study these two processes at single basepair resolution. Using a fusion protein between the heterochromatin protein Sir3 and the nonsite-specific bacterial adenine methyltransferase M.EcoGII, we mapped sites of Sir3-chromatin interactions genome-wide using long-read Nanopore sequencing to detect adenines methylated by the fusion protein and by ChIP-seq to map the distribution of Sir3-M.EcoGII. A silencing-deficient mutant of Sir3 lacking its Bromo-Adjacent Homology (BAH) domain, sir3-bah∆, was still recruited to HML, HMR, and telomeres. However, in the absence of the BAH domain, it was unable to spread away from those recruitment sites. Overexpression of Sir3 did not lead to further spreading at HML, HMR, and most telomeres. A few exceptional telomeres, like 6R, exhibited a small amount of Sir3 spreading, suggesting that boundaries at telomeres responded variably to Sir3-M.EcoGII overexpression. Finally, by using a temperature-sensitive allele of SIR3 fused to M.ECOGII, we tracked the positions first methylated after induction and found that repression of genes at HML and HMR began before Sir3 occupied the entire locus.

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Silent recognition by Toll-like receptor 5 of flagellins from human gut commensal bacteria

Project description:Flagellins from commensal bacteria can be weak Toll-like receptor (TLR)5 agonists despite high affinity binding to TLR5, ligands we termed “silent flagellins”. To determine if silent flagellins are detectable in the human gut, endogenous flagellins produced by the microbiota were isolated from stool obtained from a healthy adult female donor. TLR5 was used as bait to enrich for silent flagellins and TLR5-bound flagellins were identified by searching peptides against a custom flagellin database built from metagenome sequences.

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NGF-induced gene expression in silent nociceptors

Project description:Silent nociceptors are sensory afferents that are insensitive to noxious mechanical stimuli under normal conditions but become sensitized to such stimuli during inflammation. We had previously shown that mouse silent nociceptors express the nicotinic acetylcholine receptor alpha-3 subunit (CHRNA3) and can thus readily be identified in Tg(Chrna3-EGFP)BZ135Gsat reporter mice (Prato et al. Cell Reports 2017). Most importantly, we had shown that CHRNA3+ slient nociceptors acquire mechanosensitivity upon treatment with the inflammatory mediator nerve growth factor and demonstrated that this process requires de-novo gene transcription. Here, we performed paired-end RNA-sequencing to identify transcripts that might be involved in the acquisition of mechanosenstivity in mouse silent nociceptors.

2022-12-01 | GSE199580 | GEO

NGF-induced gene expression in silent nociceptors

Project description:NGF-induced gene expression in silent nociceptors

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Minimal requirements for the epigenetic inheritance of engineered silent chromatin domains

Project description:Mechanisms enabling genetically identical cells to differentially regulate gene expression are complex and central to organismal development and evolution. While gene silencing pathways involving DNA sequence–specific recruitment of histone-modifying enzymes are prevalent in nature, examples of sequence-independent heritable gene silencing are scarce. Studies of the fission yeast Schizosaccharomyces pombe indicate that sequence-independent propagation of heterochromatin can occur but requires numerous multisubunit protein complexes and their diverse activities. Such complexity has so far precluded a coherent articulation of the minimal requirements for heritable gene silencing by conventional in vitro reconstitution approaches. Here, we take an unconventional approach to defining these requirements by engineering sequence-independent silent chromatin inheritance in budding yeast Saccharomyces cerevisiae cells. The mechanism conferring memory upon these cells is remarkably simple and requires only two proteins, one that recognizes histone H3 lysine 9 methylation (H3K9me) and catalyzes the deacetylation of histone H4 lysine 16 (H4K16), and another that recognizes deacetylated H4K16 and catalyzes H3K9me. Together, these bilingual “read–write” proteins form an interdependent positive feedback loop that is sufficient for the transmission of DNA sequence–independent silent information over multiple generations.

2023-12-19 | GSE236173 | GEO

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