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Conserved local hypomethylation control during the bacterial cell cycle and by superimposed environmental cues

ABSTRACT: Conserved local hypomethylation control during the bacterial cell cycle and by superimposed environmental cues

PROVIDER: PRJNA317321 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3337042.fastq.gz	Fastqsanger.gz
	SRR3337043.fastq.gz	Fastqsanger.gz
	SRR3337044.fastq.gz	Fastqsanger.gz
	SRR3337045.fastq.gz	Fastqsanger.gz
	SRR3337046_subreads.fastq.gz	Fastqsanger.gz

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Conserved local hypomethylation control during the bacterial cell cycle and by superimposed environmental cues

Project description:Heritable DNA methylation imprints occur in most genomes and underlie genetic variability in humans. The mechanism and consequences of establishing and propagating local hypomethylation through consecutive rounds of DNA replication and intermittent cell division cycles are poorly understood. Our genome-wide and site-specific methyl-N6-adenine (m6A-) analyses reveal a conserved local hypomethylation mechanism in two α-proteobacterial model systems. We show that MucR, a DNA-binding protein that uses an ancestral zinc-finger fold to control expression of virulence and cell cycle genes, competes with the cell cycle-regulated adenine-methyltransferase CcrM for target sites in S-phase, but not in G1-phase. Constitutive expression of CcrM or heterologous methylases during the cell cycle homogenizes m6A patterns even when MucR is present and controls transcription. We also find that environmental responses can impose methylation remodelling at certain sites, while the conserved cell cycle circuitry imposes systemic constraints on when local hypomethylation is instated.

2016-11-28 | GSE79880 | GEO

Cell Cycle Constraints and Environmental Control of Local DNA Hypomethylation in ?-Proteobacteria.

Project description:Heritable DNA methylation imprints are ubiquitous and underlie genetic variability from bacteria to humans. In microbial genomes, DNA methylation has been implicated in gene transcription, DNA replication and repair, nucleoid segregation, transposition and virulence of pathogenic strains. Despite the importance of local (hypo)methylation at specific loci, how and when these patterns are established during the cell cycle remains poorly characterized. Taking advantage of the small genomes and the synchronizability of ?-proteobacteria, we discovered that conserved determinants of the cell cycle transcriptional circuitry establish specific hypomethylation patterns in the cell cycle model system Caulobacter crescentus. We used genome-wide methyl-N6-adenine (m6A-) analyses by restriction-enzyme-cleavage sequencing (REC-Seq) and single-molecule real-time (SMRT) sequencing to show that MucR, a transcriptional regulator that represses virulence and cell cycle genes in S-phase but no longer in G1-phase, occludes 5'-GANTC-3' sequence motifs that are methylated by the DNA adenine methyltransferase CcrM. Constitutive expression of CcrM or heterologous methylases in at least two different ?-proteobacteria homogenizes m6A patterns even when MucR is present and affects promoter activity. Environmental stress (phosphate limitation) can override and reconfigure local hypomethylation patterns imposed by the cell cycle circuitry that dictate when and where local hypomethylation is instated.

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Transcription profiling of mouse liver cells with a conditionally active liver clock to descriminate between rhythmic gene expression driven by cyclic systemic cues and local oscillators

Project description:The mammalian circadian timing system consists of a master pacemaker in the suprachiasmatic nucleus (SCN) that synchronizes self-sustained oscillators in most peripheral cells. Rhythmic gene expression in peripheral tissues can be driven by cyclic systemic cues emanating from the SCN or by local oscillators. To discriminate between these two mechanisms, we engineered a mouse strain with a conditionally active liver clock. Transcriptome profiling revealed that the circadian transcription of most genes depends on functional hepatocyte clocks. However, the expression of 31 genes, including mPer2, oscillates robustly in clock-arrested hepatocytes. Such genes may be implicated in the synchronization of liver oscillators

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Local DNA hypomethylation activates genes in rice endosperm

Project description:Cytosine methylation silences transposable elements in plants, vertebrates and fungi, but also regulates gene expression1. Plant methylation is catalyzed by three families of enzymes, each with a preferred sequence context: CG, CHG (H = A, C or T) and CHH, with CHH methylation targeted by the RNA interference (RNAi) pathway2. Arabidopsis thaliana endosperm, a placenta-like tissue that nourishes the embryo, is globally hypomethylated in the CG context while retaining high non-CG methylation3. Global methylation dynamics in seeds of cereal crops that provide the bulk of human nutrition remain unknown. Here we show that rice endosperm DNA is hypomethylated in all sequence contexts. Non-CG methylation is reduced evenly across the genome, while CG hypomethylation is localized. CHH methylation of small transposable elements is increased in embryos, suggesting that endosperm demethylation enhances transposon silencing. Genes preferentially expressed in endosperm, including those coding for major storage proteins and starch synthesizing enzymes, are frequently hypomethylated in endosperm, indicating that DNA methylation is a crucial regulator of rice endosperm biogenesis. Our data demonstrate that genome-wide reshaping of seed DNA methylation is conserved among angiosperms and has a profound effect on gene expression in cereal crops. Keywords: Epigenetics Examination of DNA methylation in rice

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AHR-TFAP2A regulates epidermal differentiation in response to environmental cues

Project description:AHR-TFAP2A regulates epidermal differentiation in response to environmental cues

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Project description:AHR-TFAP2A regulates epidermal differentiation in response to environmental cues [ChIP-seq]

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AHR-TFAP2A regulates epidermal differentiation in response to environmental cues [ChIP-seq]

Project description:The Aryl Hydrocarbon Receptor (AHR) is an environmental sensor and an indispensable regulator of epithelial homeostasis. To investigate AHR-mediated gene regulation, we performed a comprehensive transcriptomic and epigenomic analysis using human primary epidermal keratinocytes. Our results showed that AHR activation led to the induction of canonical transcription factors involved in epidermal differentiation as an early response, i.e. Transcription Factor AP-2α (TFAP2A), while epidermal differentiation-related genes, such as filaggrin and keratins, were activated as late responsive genes. The identified AHR-TFAP2A axis and its role in keratinocyte terminal differentiation was confirmed through AHR and TFAP2A knockout using CRISPR/Cas9. Our findings demonstrate that AHR regulates epidermal differentiation through the transient activation of specific transcription factors, such as TFAP2A, in response to environmental cues. The herein identified AHR-TFAP2A axis provides a promising target for the treatment of diseases related to skin barrier dysfunction.

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AHR-TFAP2A regulates epidermal differentiation in response to environmental cues [RNA-seq]

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