Abstract
Extended periods of waking result in physiological impairments in humans, rats, and flies. Sleep homeostasis, the increase in sleep observed following sleep loss, is believed to counter the negative effects of prolonged waking by restoring vital biological processes that are degraded during sleep deprivation. Sleep homeostasis, as with other behaviors, is influenced by both genes and environment. We report here that during periods of starvation, flies remain spontaneously awake but, in contrast to sleep deprivation, do not accrue any of the negative consequences of prolonged waking. Specifically, the homeostatic response and learning impairments that are a characteristic of sleep loss are not observed following prolonged waking induced by starvation. Recently, two genes, brummer (bmm) and Lipid storage droplet 2 (Lsd2), have been shown to modulate the response to starvation. bmm mutants have excess fat and are resistant to starvation, whereas Lsd2 mutants are lean and sensitive to starvation. Thus, we hypothesized that bmm and Lsd2 may play a role in sleep regulation. Indeed, bmm mutant flies display a large homeostatic response following sleep deprivation. In contrast, Lsd2 mutant flies, which phenocopy aspects of starvation as measured by low triglyceride stores, do not exhibit a homeostatic response following sleep loss. Importantly, Lsd2 mutant flies are not learning impaired after sleep deprivation. These results provide the first genetic evidence, to our knowledge, that lipid metabolism plays an important role in regulating the homeostatic response and can protect against neuronal impairments induced by prolonged waking.
Recommended Citation
M. S. Thimgan et al., "The Perilipin Homologue, Lipid Storage Droplet 2, Regulates Sleep Homeostasis and Prevents Learning Impairments following Sleep Loss," PLoS Biology, vol. 8, no. 8, PLoS, Aug 2010.
The definitive version is available at https://doi.org/10.1371/journal.pbio.1000466
Department(s)
Biological Sciences
International Standard Serial Number (ISSN)
1544-9173;1545-7885
Document Type
Article - Journal
Document Version
Final Version
File Type
text
Language(s)
English
Rights
© 2010 Thimgan et al., All rights reserved.
Creative Commons Licensing
This work is licensed under a Creative Commons Attribution 4.0 License.
Publication Date
01 Aug 2010
Comments
This study was funded in part by 1 R01 NS051305-01A1 (to PJS), WM Keck Foundation Fellowship (to MST), and the Clinical Nutrition Research Unit at Washington University grant NIH P30 DK56341.