Stress-Induced Sleep After Exposure to Ultraviolet Light Is Promoted by p53 in<i>Caenorhabditis elegans</i>

DeBardeleben, Hilary K; Lopes, Lindsey E.; Nessel, Mark P

doi:10.1534/genetics.117.300070

Cited by 46 publications

(49 citation statements)

References 71 publications

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“…Caenorhabditis elegans possess two major individual neurons that have been implicated in the induction of sleep. Cellular stress causes the secretion of EGF, which activates EGF receptor signaling in a neuron called ALA . EGF activation leads to the secretion of multiple neuropeptides from ALA, which have both overlapping and distinct inhibitory functions on behavioral activity by binding to downstream receptors, likely involving a diffusional mechanism .…”

Section: Genetically Removing Sleep In Model Systems: C Elegansmentioning

confidence: 99%

Genetic sleep deprivation: using sleep mutants to study sleep functions

Bringmann

2019

EMBO Reports

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Sleep is a fundamental conserved physiological state in animals and humans. It may serve multiple functions, ranging from energy conservation to higher brain operation. Understanding sleep functions and the underlying mechanisms requires the study of sleeplessness and its consequences. The traditional approach to remove sleep is sleep deprivation ( SD ) by sensory stimulation. However, stimulation‐induced SD can be stressful and can cause non‐specific side effects. An emerging alternative method is “genetic SD ”, which removes sleep using genetics or optogenetics. Sleep requires sleep‐active neurons and their regulators. Thus, genetic impairment of sleep circuits might lead to more specific and comprehensive sleep loss. Here, I discuss the advantages and limits of genetic SD in key genetic sleep model animals: rodents, zebrafish, fruit flies and roundworms, and how the study of genetic SD alters our view of sleep functions. Genetic SD typically causes less severe phenotypes compared with stimulation‐induced SD , suggesting that sensory stimulation‐induced SD may have overestimated the role of sleep, calling for a re‐investigation of sleep functions.

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Section: Genetically Removing Sleep In Model Systems: C Elegansmentioning

confidence: 99%

Genetic sleep deprivation: using sleep mutants to study sleep functions

Bringmann

2019

EMBO Reports

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“…We asked how cellular stress affects the C. elegans behavioral response to aversive mechanical stimuli. To induce SIS, we exposed young adult wild-type (WT) animals to UV radiation 33 . After the given exposure of UV irradiation, the animals became sterile and died within one week ( Supplementary Fig.…”

Section: Quiescence Increases After Mechanosensory Response During Uvmentioning

confidence: 99%

“…After the given exposure of UV irradiation, the animals became sterile and died within one week ( Supplementary Fig. S1), suggesting that they sustain considerable damage 33 . To track behavior, we imaged worms isolated in wells of a multi-well device (WorMotel) 34 and used frame subtraction 35 to measure behavioral activity and quiescence (see Methods).…”

Section: Quiescence Increases After Mechanosensory Response During Uvmentioning

confidence: 99%

“…Substrate vibrations elicit a mechanosensory response mediated by the gentle touch receptors 36,37 . Both chemosensory and photosensory responsiveness are known to decrease during SIS 14,33 , and mechanosensory arousability decreases in another C. elegans sleep state, developmental lethargus 38,39 . Consistent with decreased overall sensory arousability, mechanosensory responses decreased during SIS relative to controls, displaying a minimum at the time of peak quiescence (Fig.…”

Section: Quiescence Increases After Mechanosensory Response During Uvmentioning

confidence: 99%

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A quiescent state following mild sensory arousal inCaenorhabditis elegansis potentiated by stress

McClanahan

Dubuque

Kontogiorgos-Heintz

et al. 2019

Preprint

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In response to threats, animals display quiescent behaviors such as freezing and tonic immobility. How neuromodulatory states like stress affect these behaviors is not well understood. Here we describe a Caenorhabditis elegans quiescent behavior, post-response quiescence (PRQ), which is modulated by the C. elegans response to cellular stressors. Following an aversive mechanical or blue light stimulus, worms respond first by briefly moving, and then become more quiescent for a period lasting tens of seconds. PRQ occurs at low frequency in unstressed animals, but is more frequent in animals that have experienced cellular stress due to ultraviolet light exposure as well as in animals following overexpression of epidermal growth factor (EGF). PRQ requires the function of the carboxypeptidase EGL-21 and the calcium-activated protein for secretion (CAPS) UNC-31, suggesting it has a neuropeptidergic mechanism. Although PRQ requires the sleep-promoting neurons RIS and ALA, it is not accompanied by decreased arousability, and is not homeostatically regulated, suggesting that it is not a sleep state. PRQ represents a simple, tractable model for studying how neuromodulatory states alter behavioral responses to stimuli.

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“…Non-stressed males were placed onto NGM plates with OP50 as a food source at 23 o C. Starved and fasted males were placed onto NGM plates lacking peptone and any food source at times indicated and for duration indicated (18 hours or 4 hours), then analyzed or returned to NGM plates with OP50 as a food source. Heat stress was performed by placing males onto NGM plates with OP50 as a food source, setting the plate in a 37 o C incubator for 30 minutes, then returning plate to 23 o C. For ultraviolet (UV) exposure males were placed on NGM plates with a thin layer of OP50 as a food source to minimize blocking UV rays, which was set in a Spectrolinker XL-1500 (Spectroline) uncovered, and irradiated with 254 nm light using the energy input function which varies the exposure time (DeBardeleben, Lopes, Nessel, & Raizen, 2017), here set to 200 X100 µJ/cm 2 . In all non-stress and stress conditions, males were subjected to image analysis or behavioral assays at times indicated in Figures.…”

Section: Stress Inductionmentioning

confidence: 99%

Stress-induced neuron remodeling reveals differential interplay between neurexin and environmental factors

2018

Preprint

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Neurexins are neuronal adhesion molecules important for synapse maturation, function, and plasticity. Neurexins have been genetically associated with neurodevelopmental disorders including autism spectrum disorders (ASDs) and schizophrenia, but can have variable penetrance and phenotypic severity. Heritability studies indicate that a significant percentage of risk for ASD and schizophrenia includes environmental factors, highlighting the poorly understood interplay between genetic and environmental factors in pathogenesis of these disorders. The singular C. elegans ortholog of human neurexins, nrx-1, controls experience-dependent morphologic remodeling of a GABAergic neuron in adult males. Here I show that this GABAergic neuron's morphology is altered in response to each of three environmental stressors (nutritional, heat, or genotoxic stress) applied during sexual maturation, but not during adulthood. Increased outgrowth of axon-like neurites following adolescent stress results from an altered morphologic plasticity that occurs upon entry into adulthood. Despite axonal remodeling being induced by each of the three stressors, only nutritional stress (starvation) impacts behavior and is dependent on neurexin/nrx-1. Heat or genotoxic stress during sexual maturation did not alter behavior despite inducing GABAergic neuron remodeling, and this remodeling was independent of neurexin/nrx-1. Remodeling induced by starvation stress was found be dependent on neuroligin/nlg-1, the canonical binding partner for neurexin/nrx-1, as well as the stress signaling transcription factors FOXO/daf-16 and HSF1/hsf-1, each of which was also found to have unique roles in remodeling induced by heat and UV stress. The differential molecular mechanisms underlying GABAergic neuron remodeling in response to different stressors, and the disparate effects of stressors on behavior, is a novel paradigm for understanding how genetics, environmental exposures, and plasticity may contribute to brain dysfunction in ASDs and schizophrenia.

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Stress-Induced Sleep After Exposure to Ultraviolet Light Is Promoted by p53 inCaenorhabditis elegans

Cited by 46 publications

References 71 publications

Genetic sleep deprivation: using sleep mutants to study sleep functions

Genetic sleep deprivation: using sleep mutants to study sleep functions

A quiescent state following mild sensory arousal inCaenorhabditis elegansis potentiated by stress

Stress-induced neuron remodeling reveals differential interplay between neurexin and environmental factors

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