Neuronal PRDX-2-Mediated ROS Signaling Regulates Food Digestion via peripheral UPR mt Activation

All organisms depend on food digestion for survival, yet the brain-gut signaling mechanisms that regulate this process are not fully understood. Here, using an established C. elegans digestion model, we uncover a pathway in which neuronal ROS (free radicals) signal the intestine to suppress digestio...

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Bibliographic Details
Published in:Nature communications 2024-12, Vol.15 (1), p.10582
Main Authors: Liu, Yating, Li, Qian, Tian, Guojing, Zhou, Xinyi, Chen, Panpan, Chen, Bo, Shan, Zhao, Qi, Bin
Format: Article
Language:English
Subjects:
Animals
Caenorhabditis elegans - genetics
Caenorhabditis elegans - metabolism
Caenorhabditis elegans Proteins - genetics
Caenorhabditis elegans Proteins - metabolism
Digestion
Mitochondria - metabolism
Neurons - metabolism
Neuropeptides - genetics
Neuropeptides - metabolism
Peroxiredoxins - genetics
Peroxiredoxins - metabolism
Reactive Oxygen Species - metabolism
Signal Transduction
Unfolded Protein Response
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Summary:All organisms depend on food digestion for survival, yet the brain-gut signaling mechanisms that regulate this process are not fully understood. Here, using an established C. elegans digestion model, we uncover a pathway in which neuronal ROS (free radicals) signal the intestine to suppress digestion. Genetic screening reveals that reducing genes responsible for maintaining ROS balance increases free radicals and decreases digestion. PRDX-2 knockout in olfactory neurons (AWC) elevates ROS and reduces digestive capacity, mediated by the neuropeptide NLP-1 and activation of the mitochondrial unfolded protein response (UPR ) in the intestine. Additionally, over-expressing nlp-1 or ablating AWC neurons both trigger UPR and inhibit digestion. These findings reveal a brain-gut connection in which neuronal PRDX-2-mediated ROS signaling modulates food digestion, highlighting a critical role of free radicals in shutting down digestion to alleviate stress and reduce food consumption.
ISSN:2041-1723