Evidence map›Paper›PMID 32169212›Full record

ArticleCurrent biology : CB2020

Evolutionarily Conserved Regulation of Sleep by the Protein Translational Regulator PERK.

Sarah Ly, Daniel A Lee, Ewa Strus, David A Prober, Nirinjini Naidoo

Open access · bronzeAbstract read
In one paragraph

Article in Current biology : CB, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Current Evidence for Sleep States inCurrent sleep medicine reports · 2026
    Review
  5. microPublication biology · 2026
    Article
  6. Early life sleep is associated with longevity inbioRxiv : the preprint server for biology · 2025
    Article
  7. Article
  8. Article
  9. The intersection of sleep and synaptic translation in synaptic plasticity deficits in neurodevelopmental disorders.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2024
    Review
  10. Article
  11. Orthologs ofSleep advances : a journal of the Sleep Research Society · 2024
    Article
  12. Article
  13. Review
  14. Article
  15. A conserved role forSleep advances : a journal of the Sleep Research Society · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Sarah LyCenter for Sleep and Circadian Neurobiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Daniel A LeeDivision of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA.
Ewa StrusCenter for Sleep and Circadian Neurobiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
David A ProberDivision of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA.
Nirinjini NaidooCenter for Sleep and Circadian Neurobiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: naidoo@pennmedicine.upenn.edu.
University of Pennsylvania · USCalifornia Institute of Technology · US

Funding

Mechanisms of Cellular Stress-Induced SleepR01GM123783 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI NAIDOO, NIRMALA NIRINJINI, WILLIAMS, JULIE A · 2016 to 2019
$1.3M
NIGMS NIH HHS R01 GM123783
6 · The paper itself

Abstract

Sleep is a cross-species phenomenon whose evolutionary and biological function remain poorly understood. Clinical and animal studies suggest that sleep disturbance is significantly associated with disruptions in protein homeostasis-or proteostasis-in the brain, but the mechanism of this link has not been explored. In the cell, the protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) pathway modulates proteostasis by transiently inhibiting protein synthesis in response to proteostatic stress. In this study, we examined the role of the PERK pathway in sleep regulation and provide the first evidence that PERK signaling is required to regulate normal sleep in both vertebrates and invertebrates. We show that pharmacological inhibition of PERK reduces sleep in both Drosophila and zebrafish, indicating an evolutionarily conserved requirement for PERK in sleep. Genetic knockdown of PERK activity also reduces sleep in Drosophila, whereas PERK overexpression induces sleep. Finally, we demonstrate that changes in PERK signaling directly impact wake-promoting neuropeptide expression, revealing a mechanism through which proteostatic pathways can affect sleep and wake behavior. Taken together, these results demonstrate that protein synthesis pathways like PERK could represent a general mechanism of sleep and wake regulation and provide greater insight into the relationship between sleep and proteostasis.

Indexed as

Biological EvolutionAnimalsCinnamatesDrosophila melanogastereIF-2 KinaseGene Expression RegulationNeuropeptidesSignal TransductionSleepThioureaWakefulnessZebrafishZebrafish ProteinsCinnamateseIF-2 KinaseNeuropeptidessalubrinalThioureaZebrafish ProteinsDrosophilaER stressPERKprotein synthesisprotein translationproteostasissleepunfolded protein responsezebrafish

Identifiers

PMID32169212
PMCPMC8788386
OpenAlexW3011581952

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.