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...
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Published in | Nature communications Vol. 7; no. 1; p. 13234 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
08.11.2016
Nature Publishing Group Nature Portfolio |
Subjects | |
Online Access | Get full text |
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Summary: | 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 H
2
O
2
promotes, rather than compromises, sensory behavior and the function of sensory neurons such as ASH. This beneficial effect of H
2
O
2
is 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 H
2
O
2
-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.
The deleterious role of reactive oxygen species has been widely reported in the nervous system. Here the authors report that surprisingly, low doses of H
2
O
2
in fact enhances sensory neuron function and promotes sensory behaviors in
C. elegans
. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 2041-1723 2041-1723 |
DOI: | 10.1038/ncomms13234 |