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Normal sleep bouts are not essential for C. elegans survival and FoxO is important for compensatory changes in sleep

Overview of attention for article published in BMC Neuroscience, March 2018
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Title
Normal sleep bouts are not essential for C. elegans survival and FoxO is important for compensatory changes in sleep
Published in
BMC Neuroscience, March 2018
DOI 10.1186/s12868-018-0408-1
Pubmed ID
Authors

Heather L. Bennett, Yulia Khoruzhik, Dustin Hayden, Huiyan Huang, Jarred Sanders, Melissa B. Walsh, David Biron, Anne C. Hart

Abstract

Sleep deprivation impairs learning, causes stress, and can lead to death. Notch and JNK-1 pathways impact C. elegans sleep in complex ways; these have been hypothesized to involve compensatory sleep. C. elegans DAF-16, a FoxO transcription factor, is required for homeostatic response to decreased sleep and DAF-16 loss decreases survival after sleep bout deprivation. Here, we investigate connections between these pathways and the requirement for sleep after mechanical stress. Reduced function of Notch ligand LAG-2 or JNK-1 kinase resulted in increased time in sleep bouts during development. These animals were inappropriately easy to arouse using sensory stimulation, but only during sleep bouts. This constellation of defects suggested that poor quality sleep bouts in these animals might activate homeostatic mechanisms, driving compensatory increased sleep bouts. Testing this hypothesis, we found that DAF-16 FoxO function was required for increased sleep bouts in animals with defective lag-2 and jnk-1, as loss of daf-16 reduced sleep bouts back to normal levels. However, loss of daf-16 did not suppress arousal thresholds defects. Where DAF-16 function was required differed; in lag-2 and jnk-1 animals, daf-16 function was required in neurons or muscles, respectively, suggesting that disparate tissues can drive a coordinated response to sleep need. Sleep deprivation due to mechanical stimulation can cause death in many species, including C. elegans, suggesting that sleep is essential. We found that loss of sleep bouts in C. elegans due to genetic manipulation did not impact their survival, even in animals lacking DAF-16 function. However, we found that sleep bout deprivation was often fatal when combined with the concurrent stress of mechanical stimulation. Together, these results in C. elegans confirm that Notch and JNK-1 signaling are required to achieve normal sleep depth, suggest that DAF-16 is required for increased sleep bouts when signaling decreases, and that failure to enter sleep bouts is not sufficient to cause death in C. elegans, unless paired with concurrent mechanical stress. These results suggest that mechanical stress may directly contribute to death observed in previous studies of sleep deprivation and/or that sleep bouts have a uniquely restorative role in C. elegans sleep.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 43 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 43 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 9 21%
Student > Bachelor 8 19%
Researcher 7 16%
Student > Master 3 7%
Student > Postgraduate 3 7%
Other 2 5%
Unknown 11 26%
Readers by discipline Count As %
Neuroscience 9 21%
Biochemistry, Genetics and Molecular Biology 8 19%
Medicine and Dentistry 4 9%
Agricultural and Biological Sciences 3 7%
Psychology 3 7%
Other 4 9%
Unknown 12 28%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 17 May 2019.
All research outputs
#17,933,348
of 23,026,672 outputs
Outputs from BMC Neuroscience
#821
of 1,251 outputs
Outputs of similar age
#241,663
of 332,332 outputs
Outputs of similar age from BMC Neuroscience
#14
of 24 outputs
Altmetric has tracked 23,026,672 research outputs across all sources so far. This one is in the 19th percentile – i.e., 19% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,251 research outputs from this source. They receive a mean Attention Score of 4.3. This one is in the 29th percentile – i.e., 29% of its peers scored the same or lower than it.
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We're also able to compare this research output to 24 others from the same source and published within six weeks on either side of this one. This one is in the 37th percentile – i.e., 37% of its contemporaries scored the same or lower than it.