ArticleProceedings of the National Academy of Sciences of the United States of America2016
Pacemaker-neuron-dependent disturbance of the molecular clockwork by a Drosophila CLOCK mutant homologous to the mouse Clock mutation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 19 citations in OpenAlex.
- TRITHORAX and HSP68 Regulate Clock Gene Transcription in the Drosophila Transcriptional Feedback Loop.Journal of biological rhythms · 2026Article
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- Drosophila Pyruvate Kinase Links Metabolic State with Circadian Output via TARANIS and PDF.bioRxiv : the preprint server for biology · 2025Article
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- CRUMB: a shiny-based app to analyze rhythmic feeding inF1000Research · 2023Article
- Combined multiple transcriptional repression mechanisms generate ultrasensitivity and oscillations.Interface focus · 2022Article
- Systematic modeling-driven experiments identify distinct molecular clockworks underlying hierarchically organized pacemaker neurons.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- TRITHORAX-dependent arginine methylation of HSP68 mediates circadian repression by PERIOD in the monarch butterfly.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Metabolic control of daily locomotor activity mediated by tachykinin in Drosophila.Communications biology · 2021Article
- Orchestration of Circadian Timing by Macromolecular Protein Assemblies.Journal of molecular biology · 2020Review
- Periodicity, repression, and the molecular architecture of the mammalian circadian clock.The European journal of neuroscience · 2020Review
- AMP-Activated Protein Kinase Regulates Circadian Rhythm by Affecting CLOCK inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Makorin 1 Regulates Developmental Timing in Drosophila.Molecules and cells · 2018Article
- A Screening of UNF Targets IdentifiesThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Circadian clocks are composed of transcriptional/translational feedback loops (TTFLs) at the cellular level. In Drosophila TTFLs, the transcription factor dCLOCK (dCLK)/CYCLE (CYC) activates clock target gene expression, which is repressed by the physical interaction with PERIOD (PER). Here, we show that amino acids (AA) 657-707 of dCLK, a region that is homologous to the mouse Clock exon 19-encoded region, is crucial for PER binding and E-box-dependent transactivation in S2 cells. Consistently, in transgenic flies expressing dCLK with an AA657-707 deletion in the Clock (Clk(out)) genetic background (p{dClk-Δ};Clk(out)), oscillation of core clock genes' mRNAs displayed diminished amplitude compared with control flies, and the highly abundant dCLKΔ657-707 showed significantly decreased binding to PER. Behaviorally, the p{dClk-Δ};Clk(out) flies exhibited arrhythmic locomotor behavior in the photic entrainment condition but showed anticipatory activities of temperature transition and improved free-running rhythms in the temperature entrainment condition. Surprisingly, p{dClk-Δ};Clk(out) flies showed pacemaker-neuron-dependent alterations in molecular rhythms; the abundance of dCLK target clock proteins was reduced in ventral lateral neurons (LNvs) but not in dorsal neurons (DNs) in both entrainment conditions. In p{dClk-Δ};Clk(out) flies, however, strong but delayed molecular oscillations in temperature cycle-sensitive pacemaker neurons, such as DN1s and DN2s, were correlated with delayed anticipatory activities of temperature transition. Taken together, our study reveals that the LNv molecular clockwork is more sensitive than the clockwork of DNs to dysregulation of dCLK by AA657-707 deletion. Therefore, we propose that the dCLK/CYC-controlled TTFL operates differently in subsets of pacemaker neurons, which may contribute to their specific functions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.