Promotion of behavior and neuronal function by reactive oxygen species in C. elegans.
Reactive oxygen species (ROS) are well known to elicit a plethora of detrimental effects on cellular functions by causing damages to proteins, lipids and nucleic acids. Neurons are particularly vulnerable to ROS, and nearly all forms of neurodegenerative diseases are associated with oxidative stress. Here, we report the surprising finding that exposing C. elegans to low doses of H2O2promotes, rather than compromises, sensory behavior and the function of sensory neurons such as ASH. This beneficial effect of H2O2is mediated by an evolutionarily conserved peroxiredoxin-p38/MAPK signaling cascade. We further show that p38/MAPK signals to AKT and the TRPV channel OSM-9, a sensory channel in ASH neurons. AKT phosphorylates OSM-9, and such phosphorylation is required for H2O2-induced potentiation of sensory behavior and ASH neuron function. Our results uncover a beneficial effect of ROS on neurons, revealing unexpected complexity of the action of oxidative stressors in the nervous system.
College of Life Science and Technology, Collective Innovation Center for Brain Science and Key Laboratory of Molecular Biophysics of MOE, Huazhong University of Science and Technology, Wuhan, Hubei 430074, China.|Life Sciences Institute, University of Michigan, Ann Arbor, Michigan 48109, USA.
Guang
G
Li
College of Life Science and Technology, Collective Innovation Center for Brain Science and Key Laboratory of Molecular Biophysics of MOE, Huazhong University of Science and Technology, Wuhan, Hubei 430074, China.|Life Sciences Institute, University of Michigan, Ann Arbor, Michigan 48109, USA.
Jianke
J
Gong
College of Life Science and Technology, Collective Innovation Center for Brain Science and Key Laboratory of Molecular Biophysics of MOE, Huazhong University of Science and Technology, Wuhan, Hubei 430074, China.|Life Sciences Institute, University of Michigan, Ann Arbor, Michigan 48109, USA.
Haoyun
H
Lei
College of Life Science and Technology, Collective Innovation Center for Brain Science and Key Laboratory of Molecular Biophysics of MOE, Huazhong University of Science and Technology, Wuhan, Hubei 430074, China.
Jianfeng
J
Liu
Life Sciences Institute, University of Michigan, Ann Arbor, Michigan 48109, USA.|Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA.
X Z Shawn
XZ
Xu
D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects; D001522:Behavior, Animal; D017173:Caenorhabditis elegans / Q000187:drug effects / Q000201:enzymology / Q000502:physiology*; D029742:Caenorhabditis elegans Proteins / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000494:pharmacology; D020935:MAP Kinase Signaling System / Q000187:drug effects; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009474:Neurons / Q000502:physiology*; D009995:Osmosis; D054464:Peroxiredoxins / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D010769:Phosphothreonine / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012677:Sensation / Q000187:drug effects; D050916:TRPV Cation Channels / Q000378:metabolism
D029742:Caenorhabditis elegans Proteins; D009419:Nerve Tissue Proteins; C108820:OSM-9 protein, C elegans; D017382:Reactive Oxygen Species; D050916:TRPV Cation Channels; D010769:Phosphothreonine; D006861:Hydrogen Peroxide; D054464:Peroxiredoxins; D051057:Proto-Oncogene Proteins c-akt; C494915:akt-1 protein, C elegans; D020928:Mitogen-Activated Protein Kinases; C463460:Pmk-1 protein, C elegans