A Symphony of Signals: Intercellular and Intracellular Signaling Mechanisms Underlying Circadian Timekeeping in Mice and Flies

Hegazi, Sara; Lowden, Christopher; Garcia, Julian Rios; Cheng, Arthur H.; Obrietan, Karl; Levine, Joel D.; Cheng, Hai-Ying Mary

doi:10.3390/ijms20092363

Cited by 25 publications

(23 citation statements)

References 406 publications

(923 reference statements)

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“…For example, we found that Dh31 51 ; Pdf 01 double mutants, but not Dh31 51 or Pdf 01 single mutants, retain mature oocytes at 29˚C, resulting in decreased egg laying ( S5C Fig). Both Dh31 and Pdf regulate circadian rhythm [62], and Drosophila egg laying is circadian regulated [63]. Although ablation of PDF-producing neurons does not affect egg laying circadian rhythm [64], it is possible that DH31 and PDF may act in redundant pathways to regulate circadian-regulated egg-laying behavior.…”

Section: Complex Roles Of Neuropeptide Signaling In Whole-body Physiomentioning

confidence: 99%

RNAi-based screens uncover a potential new role for the orphan neuropeptide receptor Moody in Drosophila female germline stem cell maintenance

Matsuoka

Drummond‐Barbosa

2020

PLoS ONE

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Reproduction is highly sensitive to changes in physiology and the external environment. Neuropeptides are evolutionarily conserved signaling molecules that regulate multiple physiological processes. However, the potential reproductive roles of many neuropeptide signaling pathways remain underexplored. Here, we describe the results of RNAi-based screens in Drosophila melanogaster to identify neuropeptides/neuropeptide receptors with potential roles in oogenesis. The screen read-outs were either the number of eggs laid per female per day over time or fluorescence microscopy analysis of dissected ovaries. We found that the orphan neuropeptide receptor encoded by moody (homologous to mammalian melatonin receptors) is likely required in somatic cells for normal egg production and proper germline stem cell maintenance. However, the egg laying screens had low signal-to-noise ratio and did not lead to the identification of additional candidates. Thus, although egg count assays might be useful for large-scale screens to identify oogenesis regulators that result in dramatic changes in oogenesis, more labor-intensive microscopy-based screen are better applicable for identifying new physiological regulators of oogenesis with more subtle phenotypes.

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Section: Complex Roles Of Neuropeptide Signaling In Whole-body Physiomentioning

confidence: 99%

RNAi-based screens uncover a potential new role for the orphan neuropeptide receptor Moody in Drosophila female germline stem cell maintenance

Matsuoka

Drummond‐Barbosa

2020

PLoS ONE

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“…In vivo and in vitro studies of the SCN showed that calcium influx induces the activity of Ca 2+ /calmodulin-dependent protein kinase II (CaMKII), resulting in the activation of protein kinase A (PKA), and protein kinase C (PKC). These kinases then phosphorylate CREB in a circadian manner ( Agostino et al, 2004 ; Hegazi et al, 2019 ). The phosphorylated CREB translocates into the nucleus where it recognizes the CRE of the Per genes promoters and induces their expression ( Lee et al, 2010 ).…”

Section: Discussionmentioning

confidence: 99%

Calcium Sets the Clock in Ameloblasts

et al. 2020

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Background: Stromal interaction molecule 1 (STIM1) is one of the main components of the store operated Ca 2+ entry (SOCE) signaling pathway. Individuals with mutated STIM1 present severely hypomineralized enamel characterized as amelogenesis imperfecta (AI) but the downstream molecular mechanisms involved remain unclear. Circadian clock signaling plays a key role in regulating the enamel thickness and mineralization, but the effects of STIM1-mediated AI on circadian clock are unknown. Objectives: The aim of this study is to examine the potential links between SOCE and the circadian clock during amelogenesis. Methods: We have generated mice with ameloblast-specific deletion of Stim1 (Stim1 fl/fl /Amelx-iCre +/+ , Stim1 cKO) and analyzed circadian gene expression profile in Stim1 cKO compared to control (Stim1 fl/fl /Amelx-iCre −/−) using ameloblast microdissection and RNA micro-array of 84 circadian genes. Expression level changes were validated by qRT-PCR and immunohistochemistry. Results: Stim1 deletion has resulted in significant upregulation of the core circadian activator gene Brain and Muscle Aryl Hydrocarbon Receptor Nuclear Translocation 1 (Bmal1) and downregulation of the circadian inhibitor Period 2 (Per2). Our analyses also revealed that SOCE disruption results in dysregulation of two additional circadian regulators; p38α mitogen-activated protein kinase (MAPK14) and transforming growth factor-beta1 (TGF-β1). Both MAPK14 and TGF-β1 pathways are known to play major roles in enamel secretion and their dysregulation has been previously implicated in the development of AI phenotype. Conclusion: These data indicate that disruption of SOCE significantly affects the ameloblasts molecular circadian clock, suggesting that alteration of the circadian clock may be partly involved in the development of STIM1-mediated AI.

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“…In addition to VIP, other neurotransmitters such as vasopressin (AVP), gamma-aminobutyric acid (GABA), and gastrin-releasing peptide (GRP) have been described to modulate synaptic SCN coupling and activity rhythms in mice (for review, see Ref. [202]).…”

Section: Coupling Within the Scnmentioning

confidence: 99%

Coupled network of the circadian clocks: a driving force of rhythmic physiology

2020

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The circadian system is composed of coupled endogenous oscillators that allow living beings, including humans, to anticipate and adapt to daily changes in their environment. In mammals, circadian clocks form a hierarchically organized network with a ‘master clock’ located in the suprachiasmatic nucleus of the hypothalamus, which ensures entrainment of subsidiary oscillators to environmental cycles. Robust rhythmicity of body clocks is indispensable for temporally coordinating organ functions, and the disruption or misalignment of circadian rhythms caused for instance by modern lifestyle is strongly associated with various widespread diseases. This review aims to provide a comprehensive overview of our current knowledge about the molecular architecture and system‐level organization of mammalian circadian oscillators. Furthermore, we discuss the regulatory roles of peripheral clocks for cell and organ physiology and their implication in the temporal coordination of metabolism in human health and disease. Finally, we summarize methods for assessing circadian rhythmicity in humans.

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A Symphony of Signals: Intercellular and Intracellular Signaling Mechanisms Underlying Circadian Timekeeping in Mice and Flies

Cited by 25 publications

References 406 publications

RNAi-based screens uncover a potential new role for the orphan neuropeptide receptor Moody in Drosophila female germline stem cell maintenance

RNAi-based screens uncover a potential new role for the orphan neuropeptide receptor Moody in Drosophila female germline stem cell maintenance

Calcium Sets the Clock in Ameloblasts

Coupled network of the circadian clocks: a driving force of rhythmic physiology

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