ArticleNature communications2022
Neuroligin-mediated neurodevelopmental defects are induced by mitochondrial dysfunction and prevented by lutein in C. elegans.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 26 citations in OpenAlex.
- Mitochondrial complex I deficiency-associated diseases and models.Cellular and molecular life sciences : CMLS · 2026Review
- Precise subcellular organelle-targeted analyses of hepatotoxicity ofChinese herbal medicines · 2026Article
- Modeling immunoglobulin light chain amyloidosis in Caenorhabditis elegans.Disease models & mechanisms · 2025Article
- NDUFS1 upregulates ENaCα by NAD+ to promote alveolar fluid clearance in acute lung injury.International journal of medical sciences · 2025Article
- A microbiota-derived metabolite, 3-phenyllactic acid, prolongs healthspan by enhancing mitochondrial function and stress resilience via SKN-1/ATFS-1 in C. elegans.Nature communications · 2024Article
- Effects and Mechanisms of Lutein on Aging and Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- Abl depletion via autophagy mediates the beneficial effects of quercetin against Alzheimer pathology across species.Cell death discovery · 2023Article
- Article
- Synapses: The Brain's Energy-Demanding Sites.International journal of molecular sciences · 2022Review
- Expression and structural analysis of human neuroligin 2 and neuroligin 3 implicated in autism spectrum disorders.Frontiers in endocrinology · 2022Article
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
Complex-I-deficiency represents the most frequent pathogenetic cause of human mitochondriopathies. Therapeutic options for these neurodevelopmental life-threating disorders do not exist, partly due to the scarcity of appropriate model systems to study them. Caenorhabditis elegans is a genetically tractable model organism widely used to investigate neuronal pathologies. Here, we generate C. elegans models for mitochondriopathies and show that depletion of complex I subunits recapitulates biochemical, cellular and neurodevelopmental aspects of the human diseases. We exploit two models, nuo-5/NDUFS1- and lpd-5/NDUFS4-depleted animals, for a suppressor screening that identifies lutein for its ability to rescue animals' neurodevelopmental deficits. We uncover overexpression of synaptic neuroligin as an evolutionarily conserved consequence of mitochondrial dysfunction, which we find to mediate an early cholinergic defect in C. elegans. We show lutein exerts its beneficial effects by restoring neuroligin expression independently from its antioxidant activity, thus pointing to a possible novel pathogenetic target for the human disease.
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