FMRFamide-like FLP-13 Neuropeptides Promote Quiescence following Heat Stress in Caenorhabditis elegans

Nelson, Matthew D.; Lee, Kun He; Churgin, Matthew A.; Hill, Andrew J.; Buskirk, Cheryl Van; Fang-Yen, Christopher; Raizen, David M.

doi:10.1016/j.cub.2014.08.037

Cited by 109 publications

(199 citation statements)

References 21 publications

(33 reference statements)

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“…Cessation of locomotion and feeding can also be induced in adult C. elegans by satiety, stress, or genetic manipulations. Examples of the latter include heat-shock-induced activation of epidermal growth factor signaling (Van Buskirk and Sternberg 2007), mutations affecting cGMP, cAMP, or TGF-b signaling You et al 2008;Iwanir et al 2013), specific rescue of a peptidergic or insulin/insulin-like signaling pathway (Driver et al 2013;Hill et al 2014;Nagy et al 2014;Nelson et al 2014), or optogenetic activation of an avoidance response-promoting neuron (Cho and Sternberg 2014). Such findings potentially decouple worm sleep from molting.…”

Section: Worm Sleepmentioning

confidence: 99%

Sleep and Development in Genetically Tractable Model Organisms

Kayser

Biron

2016

Genetics

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Sleep is widely recognized as essential, but without a clear singular function. Inadequate sleep impairs cognition, metabolism, immune function, and many other processes. Work in genetic model systems has greatly expanded our understanding of basic sleep neurobiology as well as introduced new concepts for why we sleep. Among these is an idea with its roots in human work nearly 50 years old: sleep in early life is crucial for normal brain maturation. Nearly all known species that sleep do so more while immature, and this increased sleep coincides with a period of exuberant synaptogenesis and massive neural circuit remodeling. Adequate sleep also appears critical for normal neurodevelopmental progression. This article describes recent findings regarding molecular and circuit mechanisms of sleep, with a focus on development and the insights garnered from models amenable to detailed genetic analyses.

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Section: Worm Sleepmentioning

confidence: 99%

Sleep and Development in Genetically Tractable Model Organisms

Kayser

Biron

2016

Genetics

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“…Indeed, RIA and RIS neurons, for instance, are also involved in lethargus quiescence Turek et al 2013). Moreover, subsequent publications have shed light on perhaps a more vital role of ALA: induction of cellular stress-induced quiescence that is correlated with survival rates after cellular stress (e.g., noxious heat) Nelson et al 2014). Mutation of ceh-17, a transcription factor required for LET-23/EGFR and PLC-3/PLCg expression in ALA, and mutation of flp-13, a gene encoding FMRFamide-like neuropeptides expressed in ALA, both disrupt EGF-and cellular stress-induced quiescence.…”

Section: Discussionmentioning

confidence: 99%

“…Perhaps VAV-1 influences localization or release of FLP-13 (and/or other neuropeptides); further studies are needed to investigate these possibilities. Cellular stress induced by noxious heat causes perturbation of cellular homeostasis, which drives sleep-like behavioral quiescence Nelson et al 2014). The sleeplike behavioral quiescence induced by cellular stress results in an initial short-lived quiescent state (1 hr) followed by brief recovery and a second, prolonged quiescent state (several hours) .…”

Section: Discussionmentioning

confidence: 99%

“…In addition, lethargus quiescence is under homeostatic regulation (e.g., depriving animals in lethargus or rest by stimulation increases sleep drive), and prolonged deprivation of rest is lethal Driver et al 2013), as it is in rats (Rechtschaffen and Bergmann 2002). Recently, C. elegans has further been shown to display sleep-like quiescence following exposure to noxious stimuli that result in cellular stress Nelson et al 2014 Previously, we demonstrated that VAV-1, an evolutionarily conserved guanine nucleotide exchange factor (GEF) for Rho-family GTPases, is an important factor in a neural circuit that regulates C. elegans locomotion (Fry et al 2014). We found that VAV-1 is required in the ALA interneuron to reduce locomotory speed in active adult animals.…”

mentioning

confidence: 99%

“…In addition, lethargus quiescence is under homeostatic regulation (e.g., depriving animals in lethargus or rest by stimulation increases sleep drive), and prolonged deprivation of rest is lethal Driver et al 2013), as it is in rats (Rechtschaffen and Bergmann 2002). Recently, C. elegans has further been shown to display sleep-like quiescence following exposure to noxious stimuli that result in cellular stress Nelson et al 2014). Fascinatingly, molecules that regulate behavioral quiescence in C. elegans and Drosophila are conserved and influence sleep in mammals, indicating evolutionarily conserved origins of sleep and the potential utility of studying sleep in such simple animals Sehgal and Mignot 2011;.…”

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confidence: 99%

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A Conserved GEF for Rho-Family GTPases Acts in an EGF Signaling Pathway to Promote Sleep-like Quiescence inCaenorhabditis elegans

et al. 2016

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Sleep is evolutionarily conserved and required for organism homeostasis and survival. Despite this importance, the molecular and cellular mechanisms underlying sleep are not well understood. Caenorhabditis elegans exhibits sleep-like behavioral quiescence and thus provides a valuable, simple model system for the study of cellular and molecular regulators of this process. In C. elegans, epidermal growth factor receptor (EGFR) signaling is required in the neurosecretory neuron ALA to promote sleep-like behavioral quiescence after cellular stress. We describe a novel role for VAV-1, a conserved guanine nucleotide exchange factor (GEF) for Rho-family GTPases, in regulation of sleep-like behavioral quiescence. VAV-1, in a GEF-dependent manner, acts in ALA to suppress locomotion and feeding during sleep-like behavioral quiescence in response to cellular stress. Additionally, VAV-1 activity is required for EGF-induced sleep-like quiescence and normal levels of EGFR and secretory dense core vesicles in ALA. Importantly, the role of VAV-1 in promoting cellular stress-induced behavioral quiescence is vital for organism health because VAV-1 is required for normal survival after cellular stress.KEYWORDS behavioral quiescence; Caenorhabditis elegans; sleep; Vav D ESPITE being a subject of formal study for over 150 years, sleep is not clearly understood. Moreover, various explanations for the functional role of sleep have been proposed, such as allowing "recharging" of cells following high metabolic activity (Benington and Heller 1995;Tu and McKnight 2006;Scharf et al. 2008) and remodeling of synapses built during wakefulness (Tononi and Cirelli 2006). Yet sleep problems have a significant impact on human health and are a leading reason for seeking medical attention (Mahowald and Schenck 2005). Therefore, there is a great need for understanding the cellular and molecular mechanisms that regulate sleep-wake cycles.Simple model organisms such as Caenorhabditis elegans have the potential to provide valuable information regarding sleep regulation. C. elegans is known for its easily manipulated genetics, small nervous system with mapped neuronal connectivity, stereotypical behaviors, and the ability to be studied efficiently in large numbers. Numerous studies have shown that C. elegans lethargus, a restful period that occurs before each molt of the cuticle during larval development, is neuronally regulated and likely orthologous to sleep in mammals (Van Buskirk and Sternberg 2007;Raizen et al. 2008;Van Buskirk and Sternberg 2010;Choi et al. 2013;Iwanir et al. 2013;Turek et al. 2013;Cho and Sternberg 2014;Singh et al. 2014). Lethargus quiescence in C. elegans shares several characteristics with mammalian sleep: inactivity (decreased locomotion and cessation of pharyngeal pumping, or feeding), a specific posture, reduced response to aversive stimuli, and rapid reversibility (Cassada and Russell 1975;Raizen et al. 2008;Schwarz et al. 2012;Iwanir et al. 2013;Cho and Sternberg 2014). In addition, lethargus quiescence is under ...

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The Sleep in Caenorhabditis elegans: What We Know Until Now

Moosavi

Hatam

2017

Mol Neurobiol

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Sleep, as one of the most important requirements of our brain, has a mystical nature. Despite long-standing studies, the molecular mechanisms and physiological properties of sleep have not been defined well as the complexity of the mammals' brain make it difficult to investigate the mechanisms and properties of sleep. Although some features of sleep have changed during evolution, its existence in such a simple animal, Caenorhabditis elegans, not only signifies the importance of sleep in even simple animals, but also allows the scientist to assess the core mechanism and biological events in an uncomplicated organism. This article reviews the information which exists about the characteristics of sleep in C. elegans, its circadian rhythm, the neurons and neurotransmitters responsible for each state, and the signaling molecules involved. Although much still remains to be resolved about the sleep of C. elegans, the available knowledge helps the scientists to recognize the properties better of this mysterious function of the brain.

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FMRFamide-like FLP-13 Neuropeptides Promote Quiescence following Heat Stress in Caenorhabditis elegans

Cited by 109 publications

References 21 publications

Sleep and Development in Genetically Tractable Model Organisms

Sleep and Development in Genetically Tractable Model Organisms

A Conserved GEF for Rho-Family GTPases Acts in an EGF Signaling Pathway to Promote Sleep-like Quiescence inCaenorhabditis elegans

The Sleep in Caenorhabditis elegans: What We Know Until Now

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