New Insights into the Regulation of Heterochromatin

Wang, Jiyong; Jia, Sharon T.; Jia, Songtao

doi:10.1016/j.tig.2016.02.005

Cited by 128 publications

(117 citation statements)

References 106 publications

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“…Many other DNA and histone modifications are associated with distinct chromatin functions. For example, DNA methylation of cytosine at CpG and histone methylation of H3K9 or H3K27 are associated with active repression (Blattler and Farnham 2013; Wiles and Selker 2016; Wang, Jia, and Jia 2016), whereas CpG methylation within gene bodies prevents aberrant intragenic transcriptional initiation (Neri et al 2017). …”

Section: Epigenetic Landscapesmentioning

confidence: 99%

Metabolic and Epigenetic Coordination of T Cell and Macrophage Immunity

2017

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Recognition of pathogens by innate and adaptive immune cells instructs rapid alterations of cellular processes to promote effective resolution of infection. To accommodate increased bioenergetic and biosynthetic demands, metabolic pathways are harnessed to maximize proliferation and effector molecule production. In parallel, activation initiates context-specific gene-expression programs that drive effector functions and cell fates that correlate with changes in epigenetic landscapes. Many chromatin- and DNA-modifying enzymes make use of substrates and cofactors that are intermediates of metabolic pathways, providing potential cross talk between metabolism and epigenetic regulation of gene expression. In this review, we discuss recent studies of T cells and macrophages supporting a role for metabolic activity in integrating environmental signals with activation-induced gene-expression programs through modulation of the epigenome and speculate as to how this may influence context-specific macrophage and T cell responses to infection.

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Section: Epigenetic Landscapesmentioning

confidence: 99%

Metabolic and Epigenetic Coordination of T Cell and Macrophage Immunity

2017

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“…These domains share key features with heterochromatin in multicellular organisms, including (i) histone 3 lysine 9 (H3K9) methylation, which is catalyzed by Clr4, the homolog of human SUV39H1 and SUV39H2 enzymes; (ii) association with HP1 proteins; (iii) perinuclear clustering; and (iv) epigenetic heritability (5, 14). Two distinct mechanisms, involving the RNA interference (RNAi) machinery and site-specific DNA binding proteins, recruit Clr4 and mediate heterochromatin establishment in S. pombe (15–17).…”

mentioning

confidence: 99%

DNA sequence-dependent epigenetic inheritance of gene silencing and histone H3K9 methylation

Wang

Moazed

2017

Science

121

101

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Epigenetic inheritance mechanisms play fundamental roles in maintaining cellular memory of gene expression states. In fission yeast, histone H3 lysine 9 (H3K9) is methylated (H3K9me) at heterochromatic domains. These domains can be epigenetically inherited when epe1+, encoding an enzyme that promotes H3K9 demethylation, is deleted. How native epigenetic states are stably maintained in epe1+ cells remains unknown. Here, we developed a system to examine the role of DNA sequence and genomic context in propagation of a cis-heritable H3K9me-dependent silenced state. We show that in epe1+ cells, in addition to sequence-independent mechanisms that propagate H3K9me, epigenetic inheritance of silencing requires binding sites for sequence-dependent activating transcription factor (ATF)–adenosine 3′,5′-monophosphate (cAMP) response element–binding protein (CREB) family transcription factors within their native chromosomal context. Thus, specific DNA sequences contribute to cis inheritance of H3K9me and silent epigenetic states.

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“…Reprogramming requires intricate epigenetic mechanisms that orchestrate dynamic changes in gene expression patterns through factors involved in the assembly of “open” or “closed” chromatin domains, referred to as euchromatin or heterochromatin, respectively 5–8 . Moreover, posttranscriptional mechanisms that regulate RNA stability/degradation also control gene expression 9–12 .…”

mentioning

confidence: 99%

Iron homeostasis regulates facultative heterochromatin assembly in adaptive genome control

Larkin

Thillainadesan

Dhakshnamoorthy

et al. 2018

Nat Struct Mol Biol

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Iron metabolism is critical for sustaining life and maintaining human health. Here, we find that iron homeostasis is linked to facultative heterochromatin assembly and regulation of gene expression during adaptive genome control. We show that the fission yeast Clr4/Suv39h histone methyltransferase is part of a rheostat-like mechanism, in which transcriptional up-regulation of mRNAs in response to environmental change provides feedback to prevent their uncontrolled expression through heterochromatin assembly. Interestingly, proper iron homeostasis is required, as depletion of iron or down-regulation of iron transporters caused defects in heterochromatin assembly and unrestrained upregulation of gene expression. Remarkably, an unbiased genetic screen revealed that restoration of iron homeostasis is sufficient to re-establish facultative heterochromatin and proper gene control genome-wide. These results establish a role for iron homeostasis in facultative heterochromatin assembly and reveal a dynamic mechanism for reprogramming the genome in response to environmental changes.

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New Insights into the Regulation of Heterochromatin

Cited by 128 publications

References 106 publications

Metabolic and Epigenetic Coordination of T Cell and Macrophage Immunity

Metabolic and Epigenetic Coordination of T Cell and Macrophage Immunity

DNA sequence-dependent epigenetic inheritance of gene silencing and histone H3K9 methylation

Iron homeostasis regulates facultative heterochromatin assembly in adaptive genome control

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