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Drosophila photoreceptor chromatin accessibility landscape upon disruption of Clock activity [ClkATACseq]

ABSTRACT: Drosophila photoreceptor chromatin accessibility landscape upon disruption of Clock activity [ClkATACseq]

PROVIDER: PRJNA761801 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15827100_1.fastq.gz	Fastqsanger.gz
	SRR15827100_2.fastq.gz	Fastqsanger.gz
	SRR15827101_1.fastq.gz	Fastqsanger.gz
	SRR15827101_2.fastq.gz	Fastqsanger.gz
	SRR15827102_1.fastq.gz	Fastqsanger.gz

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Drosophila photoreceptor chromatin accessibility landscape upon disruption of Clock activity [ClkATACseq]

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Project description:Drosophila photoreceptor transcriptome landscape upon disruption of Clock activity [Rh1-ClkDN_RNA]

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Drosophila photoreceptor transcriptome landscape upon disruption of Clock activity [Rh1-ClkDN_RNA]

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Core Circadian Clock Genes Per1 and Per2 regulate the Rhythm in Photoreceptor Outer Segment Phagocytosis [Photoreceptor]

Project description:Core Circadian Clock Genes Per1 and Per2 regulate the Rhythm in Photoreceptor Outer Segment Phagocytosis [Photoreceptor]

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Interaction of Arabidopsis Cryptochrome 2 with PRR9 transmits blue light intensity fluctuation to circadian clock

Project description:Circadian pace is modulated by light intensity, known as the Aschoff’s rule, with largely unrevealed mechanisms. Here we report that photoreceptor CRY2 mediates blue light input to circadian clock by directly interacting with clock core component PRR9 in blue light dependent manner. This physical interaction dually blocks the accessibility of PRR9 protein to its co-repressor TPL/TPRs and the resulting kinase PPKs. Notably, phosphorylation of PRR9 by PPKs is critical for its DNA binding and repressive activity, hence to ensure proper circadian speed. Given the labile nature of CRY2 in strong blue light, our findings provide a mechanistic explanation for Aschoff’s rule in plants, i.e., blue light triggers CRY2 turnover in proportional to its intensity, which accordingly releasing PRR9 to fine tune circadian speed. Our findings not only reveal a novel network mediating light input into circadian clock, but also unmask a mechanism by which Arabidopsis circadian clock sensing light intensity.

2022-10-06 | PXD035252 | Pride

Clock-dependent chromatin accessibility rhythms regulate circadian transcription

Project description:Chromatin organization plays a crucial role in gene regulation by controlling the accessibility of DNA to transcription machinery. While significant progress has been made in understanding the regulatory role of clock proteins in circadian rhythms, how chromatin organization affects circadian rhythms remains poorly understood. Here, we employed ATAC-seq (Assay for Transposase-Accessible Chromatin with Sequencing) on FAC-sorted Drosophila clock neurons to assess genome-wide chromatin accessibility at dawn and dusk over the circadian cycle. We observed significant oscillations in chromatin accessibility at promoter and enhancer regions of hundreds of genes, with enhanced accessibility either at dusk or dawn, which correlated with their peak transcriptional activity. Notably, genes with enhanced accessibility at dusk were enriched with E-box motifs, while those more accessible at dawn were enriched with VRI/PDP1-box motifs, indicating that they are regulated by the core circadian feedback loops, PER/CLK and VRI/PDP1, respectively. Further, we observed a complete loss of chromatin accessibility rhythms in per01 null mutants, with chromatin consistently accessible at both dawn and dusk, underscoring the critical role of Period protein in driving chromatin compaction during the repression phase at dawn. Together, this study demonstrates the significant role of chromatin organization in circadian regulation, revealing how the interplay between clock proteins and chromatin structure orchestrates the precise timing of biological processes throughout the day. This work further implies that variations in chromatin accessibility might play a central role in the generation of diverse circadian gene expression patterns in clock neurons.

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Core Circadian Clock Genes Per1 and Per2 regulate the Rhythm in Photoreceptor Outer Segment Phagocytosis [Photoreceptor]

Project description:Retinal photoreceptors undergo daily renewal of their distal outer segments, a process indispensable for maintaining retinal health. Photoreceptor Outer Segment (POS) phagocytosis occurs as a daily peak, roughly about one hour after light onset. However, the underlying cellular and molecular mechanisms which initiate this process are still unknown. Here we show that, under constant darkness, mice deficient for core circadian clock genes (Per1 and Per2), lack a daily peak in POS phagocytosis. By qPCR analysis we found that core clock genes were rhythmic over 24h in both WT and Per1, Per2 double mutant whole retinas. More precise transcriptomics analysis of laser capture microdissected WT photoreceptors revealed no differentially expressed genes between time-points preceding and during the peak of POS phagocytosis. By contrast, we found that microdissected WT retinal pigment epithelium (RPE) had a number of genes that were differentially expressed at the peak phagocytic time-point compared to adjacent ones. We also found a number of differentially expressed genes in Per1, Per2 double mutant RPE compared to WT ones at the peak phagocytic time-point. Finally, based on STRING analysis we found a group of interacting genes which potentially drive POS phagocytosis in the RPE. This potential pathway consists of genes such as: Pacsin1, Syp, Camk2b and Camk2d among others. Our findings indicate that Per1 and Per2 are necessary clock components for driving POS phagocytosis and suggest that this process is transcriptionally driven by the RPE.

2021-06-01 | GSE172437 | GEO

Genome-wide distribution of chromatin accessibility and transcriptome of Set2-deficient Drosophila photoreceptor neurons

Project description:We report the chromatin accessibility landscape and transcriptome of Drosophila photoreceptor neurons that are Set2-deficient (via siRNA) obtained using a tissue-specific approach from 10-day old flies

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Project description:The establishment of highly accurate aging clocks based on DNA methylation highlighted the strong link between epigenetic alterations and aging. However, connecting methylation clocks to physiological changes is not straightforward. Transcriptomics and proteomics clocks on the other hand are directly connected to cellular function, yet they do not allow us to understand underlying epigenetic mechanisms. We hypothesize that chromatin accessibility, a readout that integrates many epigenetic mechanisms, may bridge epigenetic changes with their downstream effects in aging. To demonstrate that chromatin accessibility can predict age, we generated chromatin accessibility profiles from peripheral blood mononuclear cells (PBMCs) of 157 human donors, aged 20 to 74 and used them to construct a novel aging clock. Our clock predicted age with a root mean squared error of 7.69 years, a median absolute error of 5.69 years and a correlation of 0.83. Moreover, by comparing our chromatin accessibility data to matched transcriptomic profiles, we show that the genomic sites selected by our clock drive changes in transcription during aging. This chromatin accessibility clock could therefore be used to better understand the mechanisms driving the process of aging and evaluate anti-aging interventions.

2022-12-01 | GSE193140 | GEO

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