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Long non-coding RNAs have age-dependent diurnal expression that correlates with age-related changes in genome-wide facultative heterochromatin (RNA-Seq data set)

ABSTRACT: Long non-coding RNAs have age-dependent diurnal expression that correlates with age-related changes in genome-wide facultative heterochromatin (RNA-Seq data set)

PROVIDER: PRJNA432202 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6652890_1.fastq.gz	Fastqsanger.gz
	SRR6652890_2.fastq.gz	Fastqsanger.gz
	SRR6652900_1.fastq.gz	Fastqsanger.gz
	SRR6652900_2.fastq.gz	Fastqsanger.gz
	SRR6652910_1.fastq.gz	Fastqsanger.gz

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Long non-coding RNAs have age-dependent diurnal expression that correlates with age-related changes in genome-wide facultative heterochromatin (RNA-Seq data set)

Project description:The circadian rhythm controls timed choreography of gene expression to maintain normal cell physiology and metabolism. The predominant regulatory mechanism of the circadian rhythm is a transcriptional negative feedback loop that facilitates, and is facilitated by, circadian-regulated facultative heterochromatin. The long-term consequence of disrupted diurnal rhythm, or mutations in core clock genes, cause accelerated aging and an increased incidence in age-related diseases. To understand chromatin dynamics underlying age-related changes to circadian transcription, we performed a combined RNA-seq and ChIP-seq at two diurnal time-points for three different age groups. Our analysis focused on uncovering relationships between long non-coding RNA (lncRNA) and age-related changes to heterochromatin. We determined that the core clock genes maintain rhythmic expression regardless of age, but circadian output, including numerous lncRNAs, changes dramatically with age. In addition, there is both diurnal and age-related changes in Histone H3 lysine 9 tri-methylation (H3K9me3) that correlate with the changes in gene expression. Collectively, the data suggest a model where age-related changes in diurnal gene expression occur, in part, due to age-related redistribution of rhythmic facultative heterochromatin. Alterations in heterochromatin appear to be mediated by changes in diurnal lncRNA expression creating an interlocked circadian-chromatin regulatory network that undergoes age-dependent metamorphosis.

2018-01-30 | GSE109855 | GEO

Long non-coding RNAs have age-dependent diurnal expression that correlates with age-related changes in genome-wide facultative heterochromatin (ChIP-Seq data set)

2018-01-30 | GSE109854 | GEO

Long non-coding RNAs have age-dependent diurnal expression that correlates with age-related changes in genome-wide facultative heterochromatin

Project description:Long non-coding RNAs have age-dependent diurnal expression that correlates with age-related changes in genome-wide facultative heterochromatin

| PRJNA432194 | ENA

Long non-coding RNAs have age-dependent diurnal expression that correlates with age-related changes in genome-wide facultative heterochromatin (ChIP-Seq data set)

Project description:Long non-coding RNAs have age-dependent diurnal expression that correlates with age-related changes in genome-wide facultative heterochromatin (ChIP-Seq data set)

| PRJNA432201 | ENA

Long non-coding RNAs have age-dependent diurnal expression that correlates with age-related changes in genome-wide facultative heterochromatin

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-01-30 | GSE109856 | GEO

Long non-coding RNAs have age-dependent diurnal expression that coincides with age-related changes in genome-wide facultative heterochromatin.

Project description:BackgroundDisrupted diurnal rhythms cause accelerated aging and an increased incidence in age-related disease and morbidity. The circadian clock governs cell physiology and metabolism by controlling transcription and chromatin. The goal of this study is to further understand the mechanism of age-related changes to circadian chromatin with a focus on facultative heterochromatin and diurnal non-coding RNAs.ResultsWe performed a combined RNA-seq and ChIP-seq at two diurnal time-points for three different age groups to examine the connection between age-related changes to circadian transcription and heterochromatin in neuronal tissue. Our analysis focused on uncovering the relationships between long non-coding RNA (lncRNA) and age-related changes to histone H3 lysine 9 tri-methylation (H3K9me3), in part because the Period (Per) complex can direct facultative heterochromatin and models of aging suggest age-related changes to heterochromatin and DNA methylation. Our results reveal that lncRNAs and circadian output change dramatically with age, but the core clock genes remain rhythmic. Age-related changes in clock-controlled gene (ccg) expression indicate there are age-dependent circadian output that change from anabolic to catabolic processes during aging. In addition, there are diurnal and age-related changes in H3K9me3 that coincide with changes in transcription.ConclusionsThe data suggest a model where some age-related changes in diurnal expression are partially attributed to age-related alterations to rhythmic facultative heterochromatin. The changes in heterochromatin are potentially mediated by changes in diurnal lncRNA creating an interlocked circadian-chromatin regulatory network that undergoes age-dependent metamorphosis.

| S-EPMC6206985 | biostudies-literature

Diurnal cycles drive rhythmic physiology and promote survival in facultative phototrophic bacteria

Project description:Diurnal cycles drive rhythmic physiology and promote survival in facultative phototrophic bacteria

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Histone deacetylation promotes transcriptional silencing at facultative heterochromatin

Project description:It is important to accurately regulate the expression of genes involved in development and environmental response. In the fission yeast Schizosaccharomyces pombe, meiotic genes are tightly repressed during vegetative growth. Despite being embedded in heterochromatin these genes are transcribed and believed to be repressed primarily at the level of RNA. However, the mechanism of facultative heterochromatin formation and the interplay with transcription regulation is not understood. We show genome-wide that HDAC-dependent histone deacetylation is a major determinant in transcriptional silencing of facultative heterochromatin domains. Indeed, mutation of class I/II HDACs leads to increased transcription of meiotic genes and accumulation of their mRNAs. Mechanistic dissection of the pho1 gene where, in response to phosphate, transient facultative heterochromatin is established by overlapping lncRNA transcription shows that the Clr3 HDAC contributes to silencing independently of SHREC, but in an lncRNA-dependent manner. We propose that HDACs promote facultative heterochromatin by establishing alternative transcriptional silencing.

2018-03-19 | GSE108668 | GEO

Neurospora crassa genome organization requires subtelomeric facultative heterochromatin

Project description:Facultative heterochromatin in the filamentous fungus Neurospora crassa is identified by the repressive histone mark H3K27me3 and is primarily subtelomeric, while constitutive heterochromatin, marked by the DIM-5-catalzyed H3K9me3, is found at centromeres, telomeres, and smaller dispersed regions. In strains lacking constitutive heterochromatin (e.g., Δdim-5), H3K27me2/3 relocalizes to the regions formerly marked by H3K9me3. H3K27me3 is catalyzed by the SET-7 histone methyltransferase subunit of the Polycomb Repressive Complex 2 (PRC2); another PRC2 member, Neurospora p55 (NPF) regulates subtelomeric H3K27me2/3. Despite the de-repression of >70 genes, a Δset-7 strain has no distinguishable phenotype. To investigate the facultative heterochromatin contribution to genome organization, we performed high-throughput “chromosome conformation capture” (Hi-C) on mutants with impacted H3K27me2/3 deposition. A Δset-7 strain has decreased inter-/intra-subtelomeric contacts among others; this pattern is mirrored in a Δnpf strain, which lacks subtelomeric H3K27me3. In a Δset-7 strain, telomere bundles were often uncoupled from the nuclear membrane and de-repressed genes were subtelomeric. The chromosome conformation of a Δset-7;Δdim-5 double mutant was similar to Δset-7, suggesting that facultative heterochromatin relocalization does not compensate for H3K9me3 loss and rescue the Neurospora genome organization in strains with defective constitutive heterochromatin.

2016-10-27 | GSE82222 | GEO

Diurnal cycles drive rhythmic physiology and promote survival in facultative phototrophic bacteria

Project description:Bacteria have evolved many strategies to spare energy when nutrients become scarce. One widespread such strategy is facultative phototrophy, which helps heterotrophs supplement their energy supply using light. Our knowledge on the impact that such behaviors have on bacterial fitness and physiology is, however, still limited. Here, we study how a representative of the genus Porphyrobacter, in which aerobic anoxygenic phototrophy is ancestral, responds to different light regimes under nutrient limitation. We show that bacterial survival in stationary phase relies on functional reaction centers and varies depending on the light regime. Under dark‑light alternance, our bacterial model presents a diphasic life history dependent on phototrophy: during dark phases, the cells inhibit DNA replication and part of the population lyses and releases nutrients, while subsequent light phases allow for the recovery and renewed growth of the surviving cells. We correlate these cyclic variations with a pervasive pattern of rhythmic transcription which reflects global changes in diurnal metabolic activity. Finally, we demonstrate that, compared to either a phototrophy null mutant or a bacteriochlorophyll a overproducer, the wild type strain is better adapted to natural environments, where regular dark‑light cycles are interspersed with additional accidental dark episodes. Overall, our results highlight the importance of light‑induced biological rhythms in a new model of aerobic anoxygenic phototroph representative of an ecologically important group of environmental bacteria.

2023-10-12 | GSE245047 | GEO