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Stochastic models of nucleosome dynamics reveal regulatory rules of stimulus-induced epigenome remodeling

ABSTRACT: Stochastic models of nucleosome dynamics reveal regulatory rules of stimulus-induced epigenome remodeling

PROVIDER: PRJNA657750 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12465892_1.fastq.gz	Fastqsanger.gz
	SRR12465892_2.fastq.gz	Fastqsanger.gz
	SRR12465893_1.fastq.gz	Fastqsanger.gz
	SRR12465893_2.fastq.gz	Fastqsanger.gz
	SRR16844023_1.fastq.gz	Fastqsanger.gz

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Stochastic models of nucleosome dynamics reveal regulatory rules of stimulus-induced epigenome remodeling

Project description:The genomic positions of nucleosomes are a defining feature of the epigenomic state and hence of cell identity. Signal-dependent transcription factors (SDTFs), upon activation, modify the positioning of nucleosomes and cause epigenome remodeling. Here, we developed Markov models of nucleosome wrapping and unwrapping, and fit them to high resolution deep sequencing data of DNA accessibility to reveal biophysical principles of nucleosome dynamics. We found that 1) the dynamics of DNA unwrapping are significantly slower in vivo than reported from in vitro experimental data, 2) there is clear evidence for cooperativity in wrapping and unwrapping, 3) SDTF activity produced highest eviction probability when its binding site is close to but not on top of the nucleosome dyad, and 4) oscillatory SDTFs produce more variability than constant SDTF activities. Our work uncovers the regulatory rules governing nucleosome dynamics in vivo, which can predict epigenomic alterations during inflammation at single nucleosome resolution.

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Stochastic models of nucleosome dynamics reveal regulatory rules of stimulus-induced epigenome remodeling.

Project description:The genomic positions of nucleosomes are a defining feature of the cell's epigenomic state, but signal-dependent transcription factors (SDTFs), upon activation, bind to specific genomic locations and modify nucleosome positioning. Here we leverage SDTFs as perturbation probes to learn about nucleosome dynamics in living cells. We develop Markov models of nucleosome dynamics and fit them to time course sequencing data of DNA accessibility. We find that (1) the dynamics of DNA unwrapping are significantly slower in cells than reported from cell-free experiments, (2) only models with cooperativity in wrapping and unwrapping fit the available data, (3) SDTF activity produces the highest eviction probability when its binding site is adjacent to but not on the nucleosome dyad, and (4) oscillatory SDTF activity results in high location variability. Our work uncovers the regulatory rules governing SDTF-induced nucleosome dynamics in live cells, which can predict chromatin accessibility alterations during inflammation at single-nucleosome resolution.

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Epigenome wide Association and Stochastic Epigenetic Mutation analysis on cord blood of preterm birth.

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Project description:The epigenome defines the cell type, but also possesses plasticity to tune gene expression in the context of extracellular cues. This tuning is evident in immune sentinel cells such as macrophages, which respond to pathogens and cytokines with phenotypic shifts driven by epigenomic reprogramming. Recent studies indicate that this reprogramming arises from the activity of transcription factors including nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB). NFκB binds not only to available enhancers but may also produce de novo enhancers in previously silent areas of the genome. Here, we show that NFκB reprograms the macrophage epigenome in a stimulus-specific manner, in response only to a subset of pathogen-derived stimuli. The basis for these surprising differences lies in the stimulus-specific temporal dynamics of NFκB activity. In response to different stimuli, NFκB enters the nucleus with variable speed, amplitude, and duration, and may oscillate between the nucleus and cytoplasm. These dynamical features combine to specify the identity and dose of a given stimulus. We demonstrate through live cell imaging, mathematical modeling, and genetic perturbations that NFκB promotes open chromatin and formation of de novo enhancers most strongly when its dynamics are non-oscillatory. These de novo enhancers result in the activation of additional response genes. We propose a mechanistic paradigm in which the temporal dynamics of transcription factors are a key determinant of their capacity to control epigenomic reprogramming, thus enabling the formation of stimulus-specific memory in innate immune sentinel cells.

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Project description:Chromatin remodelers regulate genes by organizing nucleosomes around promoters, but their individual contributions are obfuscated by the complex in vivo milieu of factor redundancy and indirect effects. Genome-wide reconstitution of promoter nucleosome organization with purified proteins resolves this problem and is therefore a critical goal. Here we reconstitute four stages of nucleosome architecture using purified components: Yeast genomic DNA, histones, sequence-specific Abf1/Reb1, and remodelers RSC, ISW2, INO80, and ISW1a. We identify direct, specific and sufficient contributions that in vivo observations validate. First, RSC clears promoters by translating poly(dA:dT) into directional nucleosome removal. Second, partial redundancy is recapitulated where INO80 alone, or ISW2 at Abf1/Reb1sites, positions +1 nucleosomes. Third, INO80 and ISW2 each align downstream nucleosomal arrays. Fourth, ISW1a tightens the spacing to canonical repeat lengths. Such a minimal set of rules and proteins establishes core mechanisms by which promoter chromatin architecture arises through a blend of redundancy and specialization.

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