Dynamic nucleosome remodeling mediated by YY1 underlies early mouse development
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ABSTRACT:
PROVIDER: PRJNA908767 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22527055_1.fastq.gz | Fastqsanger.gz | |||
| SRR22527055_2.fastq.gz | Fastqsanger.gz | |||
| SRR22527056_1.fastq.gz | Fastqsanger.gz | |||
| SRR22527056_2.fastq.gz | Fastqsanger.gz | |||
| SRR22527057_1.fastq.gz | Fastqsanger.gz |
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Project description:Nucleosome positioning can alter the accessibility of DNA-binding proteins to their cognate DNA elements, and thus its precise control is essential for cell identity and function. Mammalian preimplantation embryos undergo temporal changes in gene expression and cell potency, suggesting the involvement of dynamic epigenetic control during this developmental phase. However, the dynamics of nucleosome organization during early development are poorly understood. In this study, using a low-input MNase-seq method, we show that nucleosome positioning is globally obscure in zygotes but becomes well defined during subsequent development. Downregulation of the chromatin assembly in embryonic stem cells can partially reverse nucleosome organization into a zygote-like pattern, suggesting that the chromatin assembly pathway might be linked to fuzzy nucleosomes in zygotes. We also reveal that YY1, a zinc finger containing transcription factor expressed upon zygotic genome activation, regulates the de novo formation of well-positioned nucleosome arrays at the regulatory elements, through identifying YY1-binding sites in 8-cell embryos. The YY1-binding regions acquire H3K27ac enrichment around the 8-cell and morula stages and YY1 depletion impairs the morula-to-blastocyst transition. Thus, our study delineates the remodeling of nucleosome organization and its underlying mechanism during early mouse development.
2023-07-16 | GSE220074 | GEO
Project description:Nucleosome positioning can alter the accessibility of DNA-binding proteins to their cognate DNA elements, and thus its precise control is essential for cell identity and function. Mammalian preimplantation embryos undergo temporal changes in gene expression and cell potency, suggesting the involvement of dynamic epigenetic control during this developmental phase. However, the dynamics of nucleosome organization during early development are poorly understood. In this study, using a low-input MNase-seq method, we show that nucleosome positioning is globally obscure in zygotes but becomes well defined during subsequent development. Down-regulation of the chromatin assembly in embryonic stem cells can partially reverse nucleosome organization into a zygote-like pattern, suggesting a possible link between the chromatin assembly pathway and fuzzy nucleosomes in zygotes. We also reveal that YY1, a zinc finger-containing transcription factor expressed upon zygotic genome activation, regulates the de novo formation of well-positioned nucleosome arrays at the regulatory elements through identifying YY1-binding sites in eight-cell embryos. The YY1-binding regions acquire H3K27ac enrichment around the eight-cell and morula stages, and YY1 depletion impairs the morula-to-blastocyst transition. Thus, our study delineates the remodeling of nucleosome organization and its underlying mechanism during early mouse development.
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Project description:Dynamic control of the accessibility of the genomic regulatory information is at the heart of stimulus-induced gene expression changes. Whereas chromatin accessibility assays describe dynamic changes in open chromatin over time, they provide only indirect and limited information on the nucleosome remodeling events that underlie such changes. Here, we combined accessibility assays and ChIP-seq on nucleosomes generated by micrococcal nuclease digestion in resting and LPS-activated macrophages. We devised a novel quantitative framework to discriminate different types of nucleosome remodeling events and used it to analyze nucleosome organization at genomic cis-regulatory elements modulated by stimulation on a genomic scale. At typical stimulus-activated enhancers, remodeling events were commonly asymmetric, with only one of the two nucleosomes flanking the central accessible region being remodeled. A systematic analysis of nucleosome organization revealed distinct associations of individual TFs with remodeling and showed that most remodeling events tended to occur early in the response and to be maintained over time, with progressively fewer novel events occurring at later times.
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Project description:Dynamic control of the accessibility of the genomic regulatory information is at the heart of stimulus-induced gene expression changes. Whereas chromatin accessibility assays describe dynamic changes in open chromatin over time, they provide only indirect and limited information on the nucleosome remodeling events that underlie such changes. Here, we combined accessibility assays and ChIP-seq on nucleosomes generated by micrococcal nuclease digestion in resting and LPS-activated macrophages. We devised a novel quantitative framework to discriminate different types of nucleosome remodeling events and used it to analyze nucleosome organization at genomic cis-regulatory elements modulated by stimulation on a genomic scale. At typical stimulus-activated enhancers, remodeling events were commonly asymmetric, with only one of the two nucleosomes flanking the central accessible region being remodeled. A systematic analysis of nucleosome organization revealed distinct associations of individual TFs with remodeling and showed that most remodeling events tended to occur early in the response and to be maintained over time, with progressively fewer novel events occurring at later times.
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Project description:The protein Yin-Yang 1 (YY1) is a ubiquitous multifunctional transcription factor. Interestingly, there are several cellular functions controlled by YY1 that could play a role in Leishmania pathogenesis. Leishmaniasis is a human disease caused by protozoan parasites of the genus Leishmania. This study examined the potential role of macrophage YY1 in promoting Leishmania intracellular survival. Knockdown of YY1 resulted in attenuated survival of Leishmania in infected macrophages, suggesting a role of YY1 in Leishmania persistence. Biochemical fractionation studies revealed Leishmania infection caused redistribution of YY1 to the cytoplasm from the nucleus where it is primarily located. Inhibition of nuclear transport by leptomycin B attenuates infection-mediated YY1 redistribution and reduces Leishmania survival. This suggests that Leishmania induces the translocation of YY1 from the nucleus to the cytoplasm of infected cells, where it may regulate host molecules to favour parasite survival. A label-free quantitative whole proteome approach showed that the expression of a large number of macrophage proteins was dependent on the YY1 level. Interestingly, several of these proteins were modulated in Leishmania-infected cells, revealing YY1-dependent host response and suggesting their potential role in Leishmania pathogenesis. Together, these findings identify YY1 as a novel and essential virulence factor by proxy that promotes Leishmania survival.
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Project description:Direct neuronal reprogramming is a promising approach to regenerate neurons from local glial cells. However, mechanisms of epigenome remodeling and co-factors facilitating this process are unclear. Here, we combine single-cell multiomics with genome-wide profiling of 3D nuclear architecture and DNA methylation in mouse astrocyte-to-neuron reprogramming mediated by Neurogenin2 (Ngn2) and its phosphorylation-resistant form (PmutNgn2), respectively. We show that Ngn2 drives multilayered chromatin remodelling at dynamic enhancer-gene interaction sites. PmutNgn2 leads to higher reprogramming efficiency and enhances epigenetic remodeling associated with neuronal maturation. However, the differences in binding sites or downstream gene activation cannot fully explain this effect. Instead, we identify Yy1, a transcriptional co-factor, recruited by direct interaction with Ngn2 to its target sites. Upon deletion of Yy1, activation of neuronal enhancers, genes, and ultimately reprogramming are impaired without affecting Ngn2 binding. Thus, our work highlights the key role of interactors of proneural factors in direct neuronal reprogramming.
2024-04-30 | GSE208742 | GEO
Project description:Dynamic control of the accessibility of the genomic regulatory information is at the heart of stimulus-induced gene expression changes. Whereas chromatin accessibility assays describe dynamic changes in open chromatin over time, they provide only indirect and limited information on the nucleosome remodeling events that underlie such changes. Here, we combined accessibility assays and ChIP-seq on nucleosomes generated by micrococcal nuclease digestion in resting and LPS-activated macrophages. We devised a novel quantitative framework to discriminate different types of nucleosome remodeling events and used it to analyze nucleosome organization at genomic cis-regulatory elements modulated by stimulation on a genomic scale. At typical stimulus-activated enhancers, remodeling events were commonly asymmetric, with only one of the two nucleosomes flanking the central accessible region being remodeled. A systematic analysis of nucleosome organization revealed distinct associations of individual TFs with remodeling and showed that most remodeling events tended to occur early in the response and to be maintained over time, with progressively fewer novel events occurring at later times.
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Project description:YY1 plays multifaceted roles in various cell types. We recently reported that YY1 regulates nucleosome organization in early mouse embryos (Sakamoto et al. Genes Dev 2023). However, despite the impaired nucleosome organization in the absence of YY1, the transcriptome was minimally affected in eight-cell embryos. We then hypothesized that YY1 might prepare a chromatin environment to regulate gene expression at later stages. To test this possibility, we performed a transcriptome analysis at the morula stage. We found that a substantial number of genes are aberrantly expressed in the absence of YY1. Furthermore, our analysis revealed that YY1 is required for the transcription of retrotransposons in early embryos.
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