The contribution of Drosophila Clk to rhythmic photoreceptor gene expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE304767 | GEO | 2026/08/31
REPOSITORIES: GEO
Similar Datasets
Project description:Rhythmic changes in the transcriptome are widespread during aging in Drosophila photoreceptors. To investigate the mechanisms underyling these rhythmic changes, we performed CUT&RUN in photoreceptors of the core transcriptional activators that control the circadian rhythm, CLK and CYC, in both young and old flies across the circadian day.
2025-12-31 | GSE253177 | GEO
Project description:The mammalian circadian clock relies on the master genes CLOCK (CLK) and BMAL1 and drives rhythmic gene expression to regulate biological functions under circadian control. We recently uncovered a surprising disconnect between the rhythmic binding of CLK:BMAL1 on DNA and the transcription of its target genes, suggesting that they are regulated by as yet uncharacterized mechanisms. Here we show that rhythmic CLK:BMAL1 DNA binding promotes rhythmic chromatin opening. The underlying mechanisms include CLK:BMAL1 binding to nucleosomes and rhythmic chromatin modifications, including the incorporation of the histone variant H2A.Z. This rhythmic chromatin remodeling mediates the rhythmic binding of other transcription factors adjacent to CLK:BMAL1, suggesting that the activity and the tissue-specific expression of these other transcription factors contribute to the genome-wide CLK:BMAL1 heterogeneous transcriptional output. These data therefore indicate that the clock regulation of transcription relies on the rhythmic regulation of chromatin accessibility and suggest that the concept of pioneer function extends to acute gene regulation, well beyond the current confines of developmental/cell specification.
2014-01-06 | GSE47144 | GEO
Project description:The mammalian circadian clock relies on the master genes CLOCK (CLK) and BMAL1 and drives rhythmic gene expression to regulate biological functions under circadian control. We recently uncovered a surprising disconnect between the rhythmic binding of CLK:BMAL1 on DNA and the transcription of its target genes, suggesting that they are regulated by as yet uncharacterized mechanisms. Here we show that rhythmic CLK:BMAL1 DNA binding promotes rhythmic chromatin opening. The underlying mechanisms include CLK:BMAL1 binding to nucleosomes and rhythmic chromatin modifications, including the incorporation of the histone variant H2A.Z. This rhythmic chromatin remodeling mediates the rhythmic binding of other transcription factors adjacent to CLK:BMAL1, suggesting that the activity and the tissue-specific expression of these other transcription factors contribute to the genome-wide CLK:BMAL1 heterogeneous transcriptional output. These data therefore indicate that the clock regulation of transcription relies on the rhythmic regulation of chromatin accessibility and suggest that the concept of pioneer function extends to acute gene regulation, well beyond the current confines of developmental/cell specification.
2014-01-06 | GSE47143 | GEO
Project description:The mammalian circadian clock relies on the master genes CLOCK (CLK) and BMAL1 and drives rhythmic gene expression to regulate biological functions under circadian control. We recently uncovered a surprising disconnect between the rhythmic binding of CLK:BMAL1 on DNA and the transcription of its target genes, suggesting that they are regulated by as yet uncharacterized mechanisms. Here we show that rhythmic CLK:BMAL1 DNA binding promotes rhythmic chromatin opening. The underlying mechanisms include CLK:BMAL1 binding to nucleosomes and rhythmic chromatin modifications, including the incorporation of the histone variant H2A.Z. This rhythmic chromatin remodeling mediates the rhythmic binding of other transcription factors adjacent to CLK:BMAL1, suggesting that the activity and the tissue-specific expression of these other transcription factors contribute to the genome-wide CLK:BMAL1 heterogeneous transcriptional output. These data therefore indicate that the clock regulation of transcription relies on the rhythmic regulation of chromatin accessibility and suggest that the concept of pioneer function extends to acute gene regulation, well beyond the current confines of developmental/cell specification.
2014-01-06 | GSE47142 | GEO
Project description:The mammalian circadian clock relies on the master genes CLOCK (CLK) and BMAL1 and drives rhythmic gene expression to regulate biological functions under circadian control. We recently uncovered a surprising disconnect between the rhythmic binding of CLK:BMAL1 on DNA and the transcription of its target genes, suggesting that they are regulated by as yet uncharacterized mechanisms. Here we show that rhythmic CLK:BMAL1 DNA binding promotes rhythmic chromatin opening. The underlying mechanisms include CLK:BMAL1 binding to nucleosomes and rhythmic chromatin modifications, including the incorporation of the histone variant H2A.Z. This rhythmic chromatin remodeling mediates the rhythmic binding of other transcription factors adjacent to CLK:BMAL1, suggesting that the activity and the tissue-specific expression of these other transcription factors contribute to the genome-wide CLK:BMAL1 heterogeneous transcriptional output. These data therefore indicate that the clock regulation of transcription relies on the rhythmic regulation of chromatin accessibility and suggest that the concept of pioneer function extends to acute gene regulation, well beyond the current confines of developmental/cell specification. Mouse liver CLK ChIP-Seq signal on Mnase-digested or sonicated chromatin, at 2 different time point (ZT22 and ZT06) from the same mice. Libraries were sequenced using Ilumina HiSeq2000. For Mnase-digested chromatin, libraries contained a mononucleosome insert (e.g., ~147bp), whereas the insert was ~150-300bp for sonicated chromatin.
2014-01-06 | E-GEOD-47144 | biostudies-arrayexpress
Project description:The mammalian circadian clock relies on the master genes CLOCK (CLK) and BMAL1 and drives rhythmic gene expression to regulate biological functions under circadian control. We recently uncovered a surprising disconnect between the rhythmic binding of CLK:BMAL1 on DNA and the transcription of its target genes, suggesting that they are regulated by as yet uncharacterized mechanisms. Here we show that rhythmic CLK:BMAL1 DNA binding promotes rhythmic chromatin opening. The underlying mechanisms include CLK:BMAL1 binding to nucleosomes and rhythmic chromatin modifications, including the incorporation of the histone variant H2A.Z. This rhythmic chromatin remodeling mediates the rhythmic binding of other transcription factors adjacent to CLK:BMAL1, suggesting that the activity and the tissue-specific expression of these other transcription factors contribute to the genome-wide CLK:BMAL1 heterogeneous transcriptional output. These data therefore indicate that the clock regulation of transcription relies on the rhythmic regulation of chromatin accessibility and suggest that the concept of pioneer function extends to acute gene regulation, well beyond the current confines of developmental/cell specification. H2A.Z ChIP-Seq signal in the mouse liver over 6 time points of the 24h light:dark cycle, in wild-type and Bmal1-/- mice. Libraries containing a mononucleosome insert were sequenced using Ilumina HiSeq2000.
2014-01-06 | E-GEOD-47143 | biostudies-arrayexpress
Project description:The mammalian circadian clock relies on the master genes CLOCK (CLK) and BMAL1 and drives rhythmic gene expression to regulate biological functions under circadian control. We recently uncovered a surprising disconnect between the rhythmic binding of CLK:BMAL1 on DNA and the transcription of its target genes, suggesting that they are regulated by as yet uncharacterized mechanisms. Here we show that rhythmic CLK:BMAL1 DNA binding promotes rhythmic chromatin opening. The underlying mechanisms include CLK:BMAL1 binding to nucleosomes and rhythmic chromatin modifications, including the incorporation of the histone variant H2A.Z. This rhythmic chromatin remodeling mediates the rhythmic binding of other transcription factors adjacent to CLK:BMAL1, suggesting that the activity and the tissue-specific expression of these other transcription factors contribute to the genome-wide CLK:BMAL1 heterogeneous transcriptional output. These data therefore indicate that the clock regulation of transcription relies on the rhythmic regulation of chromatin accessibility and suggest that the concept of pioneer function extends to acute gene regulation, well beyond the current confines of developmental/cell specification. Mouse liver nucleosome profile assayed by MNase-Seq over 6 time points of the 24h light:dark cycle (4 wild-type and 4 Bmal1-/- mice per time point). Illumina libraries containing a mononucleosome insert were sequenced using Ilumina HiSeq2000.
2014-01-06 | E-GEOD-47142 | biostudies-arrayexpress
Project description:To synchronize with environmental stimuli, predominantly light, the circadian clock directs the physiological and behavioral cycles with a periodicity of approximately 24 hours. The circadian clock is progressively dysregulated during aging, correlating with the development of many neurodegenerative diseases. Circadian disruption in the eye affects retinal development and accelerates photoreceptor degeneration during aging, which implies a protective effect of the functional circadian clock on photoreceptor neurons. At the core of the molecular clock, Clock (CLK) and Cycle (CYC), a pair of transcription activators, regulate the rhythmic transcription of output genes, including a substantial fraction of phototransduction genes. In the aging photoreceptors, CLK:CYC exhibit differential activity while the mechanisms that contribute to this change and its impact on downstream gene expression are poorly understood. H3K4me3 is a ubiquitous chromatin modification that is present at actively transcribed gene promoters. By profiling nuclear transcriptome throughout the 24h day, we identified that knockdown of any of the H3K4 methyltransferase significantly alter the rhythmic gene expression, and collectively, H3K4 methyltransferases (Set1, Trr and Trx) contribute to 90% of the rhythmic transcriptome in Drosophila photoreceptors. In addition, all of the core clock genes showed decreased expression amplitude in any of the KD conditions, indicating H3K4 methylation elevates clock-controlled transcription activation. Given that a global decrease of H3K4me3 is observed in the aging eye, our study favors the scenario where decreased H3K4me3 levels during aging reduce clock-controlled transcription.
2026-01-27 | GSE262534 | GEO
Project description:Influence of diet and neuronal clk (clock) activity on hemolymph proteomics. We have shown that as photoreceptors die (in the fly) they necrose, which results in their intercellular contents leaking into the hemolymph. We hypothesize that this process is regulated by diet and circadian clock control.
Analysis of differential protein expression in the hemolymph from flies reared on a high protein diet. Comparison of flies with and without a functional circadian clock within their photoreceptors.
Species/Strain: Drosophila, Elav-GeneSwitch-GAL4>UAS-Clk-DN1 (+/- RU486), female
2021-01-30 | MSV000086781 | MassIVE
Project description:Nearly half of the genes in the eye are regulated through the molecular circadian clock, a transcription-translation feedback loop that is governed by environmental stimuli. In aging, vision loss correlates with perturbations to the circadian clock. Rhythmic gene expression is substantially altered in the aging Drosophila melanogaster eye in that over 1/3 of genes have differential rhythmic expression. H3K4me3 is important for transcriptional activation of genes regulated by the circadian clock and is globally decreased in aging photoreceptors. It is unknown what mechanism underlies decreased H3K4me3. Glycine-N-methyltransferase (Gnmt) regulates the availability of the universal methyl donor S-adenosyl methionine (SAM) by methylating glycine to produce sarcosine and S-adenosylhomocysteine (SAH), a potent inhibitor of histone methyltransferase activity. Both Gnmt and SAH are increased in the aging eye, therefore we hypothesize that an age-dependent increase of Gnmt contributes to disruption of rhythmic gene expression. To test this hypothesis, nuclear RNA-seq was performed on photoreceptor nuclei that were collected every four hours from flies outcrossed to wild type or with overexpression of either active or partially active Gnmt
2026-03-16 | GSE267056 | GEO