Homeostasis in C. elegans sleep is characterized by two behaviorally and genetically distinct mechanisms
| العنوان: | Homeostasis in C. elegans sleep is characterized by two behaviorally and genetically distinct mechanisms |
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| المؤلفون: | Shachar Iwanir, Nora Tramm, Stanislav Nagy, Ian A Shirley, Jarred Sanders, Erel Levine, David Biron |
| المصدر: | eLife, Vol 3 (2014) eLife |
| بيانات النشر: | eLife Sciences Publications Ltd, 2014. |
| سنة النشر: | 2014 |
| مصطلحات موضوعية: | Light, 0302 clinical medicine, homeostasis, Biology (General), Caenorhabditis elegans, 0303 health sciences, Behavior, Animal, biology, General Neuroscience, General Medicine, Neuropeptide Y receptor, Sleep in non-human animals, Cell biology, C. elegans, Medicine, Signal transduction, Locomotion, Research Article, Signal Transduction, medicine.medical_specialty, insulin, QH301-705.5, Science, Posture, Neuropeptide, Inhibitory postsynaptic potential, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, Physical Stimulation, Internal medicine, medicine, Animals, quiescence, sleep, Caenorhabditis elegans Proteins, Transcription factor, neuropeptide, 030304 developmental biology, General Immunology and Microbiology, Neuropeptides, biology.organism_classification, Receptors, Neuropeptide Y, Endocrinology, Photic Stimulation, 030217 neurology & neurosurgery, Homeostasis, lethargus, Neuroscience |
| الوصف: | Biological homeostasis invokes modulatory responses aimed at stabilizing internal conditions. Using tunable photo- and mechano-stimulation, we identified two distinct categories of homeostatic responses during the sleep-like state of Caenorhabditis elegans (lethargus). In the presence of weak or no stimuli, extended motion caused a subsequent extension of quiescence. The neuropeptide Y receptor homolog, NPR-1, and an inhibitory neuropeptide known to activate it, FLP-18, were required for this process. In the presence of strong stimuli, the correlations between motion and quiescence were disrupted for several minutes but homeostasis manifested as an overall elevation of the time spent in quiescence. This response to strong stimuli required the function of the DAF-16/FOXO transcription factor in neurons, but not that of NPR-1. Conversely, response to weak stimuli did not require the function of DAF-16/FOXO. These findings suggest that routine homeostatic stabilization of sleep may be distinct from homeostatic compensation following a strong disturbance. DOI: http://dx.doi.org/10.7554/eLife.04380.001Test eLife digest The regenerative properties of sleep are required by all animals, with even the simplest animal, the nematode Caenorhabditis elegans, displaying a sleep-like state called lethargus. During development, nematodes must pass through four larval stages en route to adulthood, and the end of each stage is preceded by a period of lethargus lasting 2 to 3 hr. Human sleep is divided into distinct stages that recur in a prescribed order throughout the night. Nematodes, on the other hand, simply experience alternating periods of activity and stillness as they sleep. Nevertheless, in both species, any disruptions to sleep automatically lead to adjustments of the rest of the sleep cycle to compensate for the disturbance and to ensure that the organism gets an adequate amount of sleep overall. To date, it has been assumed that a single mechanism is responsible for adjusting the sleep cycle after any disturbance, regardless of its severity. However, Nagy, Tramm, Sanders et al. now show that this is not the case in C. elegans. Sleeping nematodes that were lightly disturbed by exposing them to light or to vibrations—causing them to briefly increase their activity levels—compensated for the disturbance by lengthening their next inactive period. By contrast, worms that were vigorously agitated by stronger vibrations showed a different response: the alternating pattern of stillness and activity was disrupted for several minutes, followed by an overall increase in the length of time spent in the stillness phase. Experiments using genetically modified worms revealed that these two responses involve distinct molecular pathways. A signaling molecule called neuropeptide Y affects the response to minor sleep disruptions, whereas a transcription factor called DAF-16/FOXO is involved in the corresponding role after major disruptions. Given that neuropeptide Y has already been implicated in sleep regulation in humans and flies, it is not implausible that similar mechanisms may occur in response to disturbances of our own sleep. DOI: http://dx.doi.org/10.7554/eLife.04380.002Test |
| اللغة: | English |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::bbb864f6c32d83ce774257d399fc44a8Test https://elifesciences.org/articles/04380Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....bbb864f6c32d83ce774257d399fc44a8 |
| قاعدة البيانات: | OpenAIRE |
| الوصف غير متاح. |