Promotion of behavior and neuronal function by reactive oxygen species in C. elegans
Citations Over TimeTop 11% of 2016 papers
Abstract
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 H2O2 promotes, rather than compromises, sensory behavior and the function of sensory neurons such as ASH. This beneficial effect of H2O2 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 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.
Related Papers
- → Phosphorylation of PI3K/Akt and MAPK/ERK in an early entry step of enterovirus 71(2005)114 cited
- 2,3,7,8-Tetrachlorodibenzo-p-dioxin activates ERK and p38 mitogen-activated protein kinases in RAW 264.7 cells.(2005)
- → Biogenic nanoselenium particles activate Nrf2‐ARE pathway by phosphorylating p38, ERK1/2, and AKT on IPEC‐J2 cells(2018)27 cited
- → Influence of aging and calorie restriction on MAPKs activity in rat kidney(2002)74 cited
- p38 MAPK involves in cepharanthine -induced apoptosis in cardiomyocytes(2011)