scholarly journals Artificial Light at Night Influences Clock-Gene Expression, Activity, and Fecundity in the Mosquito Culex pipiens f. molestus

2019 ◽  
Vol 11 (22) ◽  
pp. 6220 ◽  
Author(s):  
Honnen ◽  
Kypke ◽  
Hölker ◽  
Monaghan

Light is an important environmental cue, and exposure to artificial light at night (ALAN) may disrupt organismal physiology and behavior. We investigated whether ALAN led to changes in clock-gene expression, diel activity patterns, and fecundity in laboratory populations of the mosquito Culex pipiens f. molestus (Diptera, Culicidae), a species that occurs in urban areas and is thus regularly exposed to ALAN. Populations were kept under 16hours (h):8h light:dark cycles or were subjected to an additional 3.5 h of light (100–300 lx) in the evenings. ALAN induced significant changes in expression in all genes studied, either alone (period) or as an interaction with time (timeless, cryptochrome2, Clock, cycle). Changes were sex-specific: period was down-regulated in both sexes, cycle was up-regulated in females, and Clock was down-regulated in males. ALAN-exposed mosquitoes were less active during the extra-light phase, but exposed females were more active later in the night. ALAN-exposed females also produced smaller and fewer eggs. Our findings indicate a sex-specific impact of ALAN on the physiology and behavior of Culex pipiens f. molestus and that changes in clock-gene expression, activity, and fecundity may be linked.

2020 ◽  
Author(s):  
Davide M. Dominoni ◽  
Maaike de Jong ◽  
Kees van Oers ◽  
Peter O’Shaughnessy ◽  
Gavin Blackburn ◽  
...  

AbstractGlobally increasing levels of artificial light at night (ALAN) have been associated with shifts in behavioral rhythms of many wild organisms. It is however unknown to what extent this change in behavior is due to shifts in the circadian clock, and, importantly, whether the physiological pathways orchestrated by the circadian clock are desynchronized by ALAN. Such circadian disruption could have severe consequences for wildlife health, as shown for humans. Here, we analyze the effects of experimental ALAN on rhythmic behavior, gene expression and metabolomic profiles in a wild songbird, the great tit (Parus major). We exposed 34 captive males to three ALAN intensities or to dark nights and recorded their activity rhythms. After three weeks, we collected mid-day and midnight samples of hypothalamus, hippocampus, liver, spleen and plasma. ALAN advanced wake-up time, and this shift was paralleled by an advance in hypothalamic expression of the clock gene BMAL1, which is key to integrating physiological pathways. BMAL1 advances were remarkably consistent across tissues, suggesting close links of brain and peripheral clock gene expression with activity rhythms. However, only a minority of other candidate genes (4 out of 12) paralleled the shifted BMAL1 expression. Moreover, metabolomic profiling showed that only 9.7% of the 755 analyzed metabolites followed the circadian shift. Thus, despite the shifted timing of key clock functions under ALAN, birds suffered internal desynchronization. We thus suggest circadian disruption to be a key link between ALAN and health impacts, in birds and humans alike.Significance StatementShifts in daily activity are a common consequence of artificial light at night (ALAN). In humans, shifted activity cycles often become desynchronized from internal physiological rhythms, with serious health implications. To what extent a similar desynchronization occurs in wild animals experiencing ALAN is currently unknown. We exposed captive great tits to increasing levels of LAN, and found that activity patterns and a core clock gene, BMAL1, shifted in concert. However, only a minority of additional candidate genes and less than 10% of the metabolites followed this circadian shift, suggesting internal desynchronization of physiological rhythms. Our study emphasizes the massive potential for ALAN to impact the health of wild animals through circadian disruption.


2012 ◽  
Vol 113 (3) ◽  
pp. 385-392 ◽  
Author(s):  
Hélène Hadden ◽  
Steven J. Soldin ◽  
Donald Massaro

Most aspects of human physiology and behavior exhibit 24-h rhythms driven by a master circadian clock in the brain, which synchronizes peripheral clocks. Lung function and ventilation are subject to circadian regulation and exhibit circadian oscillations. Sleep disruption, which causes circadian disruption, is common in those with chronic lung disease, and in the general population; however, little is known about the effect on the lung of circadian disruption. We tested the hypothesis circadian disruption alters expression of clock genes in the lung and that this is associated with altered lung mechanics. Female and male mice were maintained on a 12:12-h light/dark cycle (control) or exposed for 4 wk to a shifting light regimen mimicking chronic jet lag (CJL). Airway resistance (Rn), tissue damping (G), and tissue elastance (H) did not differ between control and CJL females. Rn at positive end-expiratory pressure (PEEP) of 2 and 3 cmH2O was lower in CJL males compared with controls. G, H, and G/H did not differ between CJL and control males. Among CJL females, expression of clock genes, Bmal1 and Rev-erb alpha, was decreased; expression of their repressors, Per2 and Cry 2, was increased. Among CJL males, expression of Clock was decreased; Per 2 and Rev-erb alpha expression was increased. We conclude circadian disruption alters lung mechanics and clock gene expression and does so in a sexually dimorphic manner.


2004 ◽  
Vol 120 (2) ◽  
pp. 164-172 ◽  
Author(s):  
V Simonneaux ◽  
V.-J Poirel ◽  
M.-L Garidou ◽  
D Nguyen ◽  
E Diaz-Rodriguez ◽  
...  

Cephalalgia ◽  
2017 ◽  
Vol 38 (3) ◽  
pp. 496-502 ◽  
Author(s):  
Carmen Fourier ◽  
Caroline Ran ◽  
Margret Zinnegger ◽  
Anne-Sofie Johansson ◽  
Christina Sjöstrand ◽  
...  

Background Cluster headache is characterized by recurrent unilateral headache attacks of severe intensity. One of the main features in a majority of patients is a striking rhythmicity of attacks. The CLOCK ( Circadian Locomotor Output Cycles Kaput) gene encodes a transcription factor that serves as a basic driving force for circadian rhythm in humans and is therefore particularly interesting as a candidate gene for cluster headache. Methods We performed an association study on a large Swedish cluster headache case-control sample (449 patients and 677 controls) screening for three single nucleotide polymorphisms (SNPs) in the CLOCK gene implicated in diurnal preference (rs1801260) or sleep duration (rs11932595 and rs12649507), respectively. We further wanted to investigate the effect of identified associated SNPs on CLOCK gene expression. Results We found a significant association with rs12649507 and cluster headache ( p = 0.0069) and this data was strengthened when stratifying for reported diurnal rhythmicity of attacks ( p = 0.0009). We investigated the effect of rs12649507 on CLOCK gene expression in human primary fibroblast cultures and identified a significant increase in CLOCK mRNA expression ( p = 0.0232). Conclusions Our results strengthen the hypothesis of the involvement of circadian rhythm in cluster headache.


2021 ◽  
Vol 18 (182) ◽  
pp. 20210454
Author(s):  
Natthapong Sueviriyapan ◽  
Daniel Granados-Fuentes ◽  
Tatiana Simon ◽  
Erik D. Herzog ◽  
Michael A. Henson

In the suprachiasmatic nucleus (SCN), γ-aminobutyric acid (GABA) is a primary neurotransmitter. GABA can signal through two types of GABA A receptor subunits, often referred to as synaptic GABA A (gamma subunit) and extra-synaptic GABA A (delta subunit). To test the functional roles of these distinct GABA A in regulating circadian rhythms, we developed a multicellular SCN model where we could separately compare the effects of manipulating GABA neurotransmitter or receptor dynamics. Our model predicted that blocking GABA signalling modestly increased synchrony among circadian cells, consistent with published SCN pharmacology. Conversely, the model predicted that lowering GABA A receptor density reduced firing rate, circadian cell fraction, amplitude and synchrony among individual neurons. When we tested these predictions, we found that the knockdown of delta GABA A reduced the amplitude and synchrony of clock gene expression among cells in SCN explants. The model further predicted that increasing gamma GABA A densities could enhance synchrony, as opposed to increasing delta GABA A densities. Overall, our model reveals how blocking GABA A receptors can modestly increase synchrony, while increasing the relative density of gamma over delta subunits can dramatically increase synchrony. We hypothesize that increased gamma GABA A density in the winter could underlie the tighter phase relationships among SCN cells.


2014 ◽  
Vol 125 (3) ◽  
pp. 329-332 ◽  
Author(s):  
Shunpei Moriya ◽  
Yu Tahara ◽  
Hiroyuki Sasaki ◽  
Yutaro Hamaguchi ◽  
Daisuke Kuriki ◽  
...  

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