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Examining the Effect of Pesticides on Caenorhabditis elegans Neurons
Published on: May 27, 2022
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Bacterially produced metabolites protect C. elegans neurons from degeneration
Arles Urrutia1,2, Víctor A García-Angulo2,3, Andrés Fuentes2
1Centro Interdisciplinario de Neurociencia de Valparaíso, Facultad de Ciencias, Universidad de Valparaíso, Valparaíso, Chile.
Plos Biology
|March 26, 2020
Summary
Dietary bacteria significantly impact neurodegeneration in C. elegans. The E. coli HT115 strain offers substantial neuroprotection, mediated by GABA and lactate, highlighting diet
Area of Science:
- Neuroscience
- Microbiology
- Genetics
Background:
- The gut microbiota plays a crucial role in host physiology.
- Dietary components influence host health, but their impact on neuronal survival is less understood.
- Caenorhabditis elegans fed specific bacteria provides a model to study diet-microbiota-host interactions.
Purpose of the Study:
- To investigate the effect of different bacterial diets on neurodegeneration in C. elegans.
- To identify bacterial metabolites responsible for neuroprotection.
- To elucidate the molecular mechanisms underlying diet-mediated neuroprotection.
Main Methods:
- Utilized a C. elegans model expressing a neurotoxic allele (MEC-4d) to study touch receptor neuron (TRN) degeneration.
- Compared neurodegeneration rates across various bacterial diets, including Escherichia coli OP50 and HT115.
- Employed transcriptomics, metabolomics, and genetic analysis (daf-16 loss-of-function, gad mutants) to identify protective mechanisms.
- Investigated the role of GABA and lactate supplementation and specific C. elegans GABA transporters and receptors.
Main Results:
- Escherichia coli HT115 significantly reduced TRN degeneration compared to E. coli OP50, offering over 40% neuroprotection.
- Neuroprotection was long-lasting, not restricted to TRNs, and could be induced by UV-killed HT115 or co-feeding with OP50.
- HT115 diet promoted DAF-16 nuclear translocation, a known neuroprotective pathway.
- Bacterial metabolites γ-aminobutyric acid (GABA) and lactate were identified as key protective factors.
- GABA production by HT115, mediated by glutamate decarboxylase (gad) genes, was essential for neuroprotection.
- Lactate supplementation also enhanced neuronal survival.
Conclusions:
- Dietary bacteria, particularly E. coli HT115, can confer significant neuroprotection in C. elegans.
- Bacterially produced GABA and lactate are crucial mediators of this neuroprotective effect.
- The findings highlight the importance of neuroactive dietary compounds in maintaining nervous system homeostasis and suggest potential therapeutic avenues for neurodegenerative diseases.
