ERK phosphorylation regulates sleep and plasticity in Drosophila.
Given the relationship between sleep and plasticity, we examined the role of Extracellular signal-regulated kinase (ERK) in regulating baseline sleep, and modulating the response to waking experience. Both sleep deprivation and social enrichment increase ERK phosphorylation in wild-type flies. The effects of both sleep deprivation and social enrichment on structural plasticity in the LNvs can be recapitulated by expressing an active version of ERK (UAS-ERK(SEM)) pan-neuronally in the adult fly using GeneSwitch (Gsw) Gsw-elav-GAL4. Conversely, disrupting ERK reduces sleep and prevents both the behavioral and structural plasticity normally induced by social enrichment. Finally, using transgenic flies carrying a cAMP response Element (CRE)-luciferase reporter we show that activating ERK enhances CRE-Luc activity while disrupting ERK reduces it. These data suggest that ERK phosphorylation is an important mediator in transducing waking experience into sleep.
Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America ; Department of Anatomy, Washington University Medical School, Saint Louis, Missouri, United States of America.
William M
WM
Vanderheyden
Jason R
JR
Gerstner
Anne
A
Tanenhaus
Jerry C
JC
Yin
Paul J
PJ
Shaw
D000818:Animals; D030801:Animals, Genetically Modified; D004330:Drosophila / Q000201:enzymology* / Q000378:metabolism / Q000502:physiology*; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism; D048049:Extracellular Signal-Regulated MAP Kinases / Q000235:genetics / Q000378:metabolism*; D010766:Phosphorylation; D012890:Sleep / Q000502:physiology
D029721:Drosophila Proteins; D048049:Extracellular Signal-Regulated MAP Kinases