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Iron-dependent H3K9me demethylation during B cell activation and proliferation

ABSTRACT: Iron-dependent H3K9me demethylation during B cell activation and proliferation

PROVIDER: PRJNA544500 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9114906.fastq.gz	Fastqsanger.gz
	SRR9114907.fastq.gz	Fastqsanger.gz
	SRR9114908.fastq.gz	Fastqsanger.gz

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Iron-dependent H3K9me demethylation during B cell activation and proliferation

Project description:To explore whether iron is required for BCR-induced H3K9 demethylation during B cell activation, we performed ChIP-seq to check the H3K9me2 modification in control (iron-normal) and iron-deficient B cells

2019-05-24 | GSE131716 | GEO

PHF2-mediated H3K9me balance orchestrates heterochromatin stability and progenitor proliferation in early neurogenesisPHF2-mediated H3K9me balance orchestrates heterochromatin stability and progenitor proliferation in early neurogenesis

Project description:Heterochromatin stability is crucial for progenitor proliferation during early neurogenesis. It relays on the maintenance of local hubs of H3K9me. However, the current understanding of the processes involved in the formation of efficient localized levels of H3K9me remains limited. To address this intriguing question, we used a neural stem cell (NSC) to analyze the function of the H3K9me2 demethylase PHF2, which is crucial for progenitor proliferation. Through mass spectroscopy and genome-wide assays, we uncovered that PHF2 interacts with heterochromatin components and it is enriched at pericentromeric heterochromatin (PcH) boundaries. This binding is essential for maintaining silenced the satellite repeats thereby preventing DNA damage and genome instability. Depletion of PHF2 led to increased transcription of heterochromatic repeats, accompanied by a decrease in H3K9me3 levels and alterations in PcH organization. Further analysis revealed that PHF2's PHD and catalytic domains are crucial for maintaining PcH stability and preventing unscheduled repeat transcription, thereby safeguarding genome integrity. These results highlight the multifaceted nature of PHF2's functions in maintaining heterochromatin stability and regulating gene expression during neural development. Altogether, our study unravels the intricate relationship between heterochromatin stability and progenitor proliferation during mammalian neurogenesis, shedding light on its potential as a therapeutic target for neurodevelopmental disorders

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Discovery, characterization, and metabolic engineering of Rieske non-heme iron monooxygenases for guaiacol O-demethylation

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Iron Drives Anabolic Metabolism Through Active Histone Demethylation and mTORC1

Project description:All living cells require a minimal iron threshold to sustain anabolic metabolism. However, the mechanisms by which cells sense iron to regulate anabolic processes are unclear. Here, we report a universal eukaryotic pathway for iron sensing in which molecular iron is required to sustain active histone demethylation and maintain the expression of critical components of the pro-anabolic mTORC1 pathway. Specifically, we identify the iron-binding histone-demethylase KDM3B as an intrinsic iron sensor that regulates mTORC1 activity by demethylating H3K9me2 at enhancers of a high-affinity leucine transporter and RAPTOR. By directly suppressing leucine availability and RAPTOR levels, iron deficiency (ID) supersedes other nutrient inputs into mTORC1. This process occurs in vivo, and is not an indirect effect by canonical iron-utilizing pathways. These data demonstrate a novel mechanism of eukaryotic iron sensing through dynamic chromatin remodeling and repression of mTORC1 mediated anabolism. Due to ancestral eukaryotes sharing homologues of KDMs and mTORC1 core components, this pathway likely predated the emergence of the other kingdom-specific nutrient sensors for mTORC1.

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cAMP Signaling Regulates DNA Demethylation by Augmenting the Intracellular Labile Ferrous Iron Pool

Project description:In this study we show that cAMP helps regulate cytosine demethylation through augmenting the intracellular labile ferrous iron pool.

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Iron Drives Anabolic Metabolism Through Active Histone Demethylation and mTORC1

Project description:All living cells require a minimal iron threshold to sustain anabolic metabolism. However, the mechanisms by which cells sense iron to regulate anabolic processes are unclear. Here, we report a universal eukaryotic pathway for iron sensing in which molecular iron is required to sustain active histone demethylation and maintain the expression of critical components of the pro-anabolic mTORC1 pathway. Specifically, we identify the iron-binding histone-demethylase KDM3B as an intrinsic iron sensor that regulates mTORC1 activity by demethylating H3K9me2 at enhancers of genes encoding high-affinity leucine transporters and RAPTOR. By directly suppressing leucine availability and RAPTOR levels, iron deficiency (ID) supersedes other nutrient inputs into mTORC1. This process occurs in vivo, and is not an indirect effect by canonical iron-utilizing pathways. Elevated expression of KDM3B targets is associated with reduced survival in a subset of human cancers and ID represses mTORC1 in patient-derived tumor cells and sensitizes cancer cells to chemotherapy. These data demonstrate a novel mechanism of eukaryotic iron sensing through dynamic chromatin remodeling and repression of mTORC1 mediated anabolism. Due to ancestral eukaryotes sharing homologues of KDMs and mTORC1 core components, this pathway likely predated the emergence of the other kingdom-specific nutrient sensors for mTORC1

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Iron Drives Anabolic Metabolism Through Active Histone Demethylation and mTORC1

Project description:Iron Drives Anabolic Metabolism Through Active Histone Demethylation and mTORC1

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Iron-dependent histone 3 lysine 9 demethylation controls B cell proliferation and humoral immune responses.

Project description:Trace elements play important roles in human health, but little is known about their functions in humoral immunity. Here, we show an important role for iron in inducing cyclin E and B cell proliferation. We find that iron-deficient individuals exhibit a significantly reduced antibody response to the measles vaccine when compared to iron-normal controls. Mice with iron deficiency also exhibit attenuated T-dependent or T-independent antigen-specific antibody responses. We show that iron is essential for B cell proliferation; both iron deficiency and α-ketoglutarate inhibition could suppress cyclin E1 induction and S phase entry of B cells upon activation. Finally, we demonstrate that three demethylases, KDM2B, KDM3B and KDM4C, are responsible for histone 3 lysine 9 (H3K9) demethylation at the cyclin E1 promoter, cyclin E1 induction and B cell proliferation. Thus, our data reveal a crucial role of H3K9 demethylation in B cell proliferation, and the importance of iron in humoral immunity.

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Fission yeasts CENPA and H3K9me Chip-seq

Project description:Fission yeasts CENPA and H3K9me Chip-seq

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H3K9me blocks transcription factor activity in differentiated cells to ensure tissue integrity [RNA-seq]

Project description:Development in multicellular organisms is governed by a carefully orchestrated program of gene expression controlled by both genetic and epigenetic factors1,2. Histone H3 lysine 9 methylation (H3K9me) is the defining modification of heterochromatin, which is thought to have two main functions. It silences satellite repeats and transposable elements to ensure genome stability3, and stabilizes differentiated states by repressing tissue-specific genes4,5. Not surprisingly, the loss of appropriately targeted heterochromatin is associated with cancer, loss of tissue integrity, and aging5-8. How H3K9me restricts transcription is unknown. Here we show that in C. elegans H3K9me2 is required to silence different sets of genes in embryos and differentiated post-mitotic cells. During nematode development H3K9me is lost from genes that define cell-type identity and is gained at genes expressed at prior stages or in alternative tissues. We found that a continuous deposition of H3K9me2 is necessary to maintain silencing in terminally differentiated cells. Its loss leads to DNA decompaction, but this is not sufficient to derepress H3K9me-marked genes. Instead, gene derepression in differentiated tissues requires distinct sets of transcription factors (TF) that aberrantly activate enhancers or promoters. Tissue-specific H3K9me distribution thus contributes critically to cell-type specific TF binding providing a rationale for how a limited set of TFs can control complex organismal development9,10.

2021-08-01 | GSE167167 | GEO

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