ArticleThe Journal of biological chemistry2015
Comparative Metabolomic Profiling Reveals That Dysregulated Glycolysis Stemming from Lack of Salvage NAD+ Biosynthesis Impairs Reproductive Development in Caenorhabditis elegans.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Histone methyltransferase SET-18/SMYD2-mediated activation of NADase TIR-1d/SARM1 increases mtROS to promote aging.iScience · 2026Article
- De novo NADCommunications biology · 2025Article
- NAMPT-dependent NADProceedings of the National Academy of Sciences of the United States of America · 2023Article
- NADThe Journal of reproduction and development · 2022Review
- Quo VadisMetabolites · 2021Review
- Effects of NADBiomolecules · 2020Review
- Genetic and functional diversification of chemosensory pathway receptors in mosquito-borne filarial nematodes.PLoS biology · 2020Article
- Organ-specific effects on glycolysis by the dioxin-activated aryl hydrocarbon receptor.PloS one · 2020Article
- The role of poly(ADP-ribose) polymerases in manganese exposed Caenorhabditis elegans.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2020Article
- Nicotinamide Inhibits Aphid Fecundity and Impacts Survival.Scientific reports · 2019Article
- IDH-1 deficiency induces growth defects and metabolic alterations in GSPD-1-deficient Caenorhabditis elegans.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Expanded genetic screening ineLife · 2018Article
- Lipidomic Analysis ofBio-protocol · 2017Article
- Knock-out of a mitochondrial sirtuin protects neurons from degeneration in Caenorhabditis elegans.PLoS genetics · 2017Article
- Uridine monophosphate synthetase enables eukaryoticThe Journal of biological chemistry · 2017Article
- Cardiomyocyte Differentiation Promotes Cell Survival During Nicotinamide Phosphoribosyltransferase Inhibition Through Increased Maintenance of Cellular Energy Stores.Stem cells translational medicine · 2017Article
- Nicotinamide is an endogenous agonist for a C. elegans TRPV OSM-9 and OCR-4 channel.Nature communications · 2016Article
- NAD+ Supplementation Attenuates Methylmercury Dopaminergic and Mitochondrial Toxicity in Caenorhabditis Elegans.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
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Authors and funding
11 authors.
Funding
Abstract
Temporal developmental progression is highly coordinated in Caenorhabditis elegans. However, loss of nicotinamidase PNC-1 activity slows reproductive development, uncoupling it from its typical progression relative to the soma. Using LC/MS we demonstrate that pnc-1 mutants do not salvage the nicotinamide released by NAD(+) consumers to resynthesize NAD(+), resulting in a reduction in global NAD(+) bioavailability. We manipulate NAD(+) levels to demonstrate that a minor deficit in NAD(+) availability is incompatible with a normal pace of gonad development. The NAD(+) deficit compromises NAD(+) consumer activity, but we surprisingly found no functional link between consumer activity and reproductive development. As a result we turned to a comparative metabolomics approach to identify the cause of the developmental phenotype. We reveal widespread metabolic perturbations, and using complementary pharmacological and genetic approaches, we demonstrate that a glycolytic block accounts for the slow pace of reproductive development. Interestingly, mitochondria are protected from both the deficiency in NAD(+) biosynthesis and the effects of reduced glycolytic output. We suggest that compensatory metabolic processes that maintain mitochondrial activity in the absence of efficient glycolysis are incompatible with the requirements for reproductive development, which requires high levels of cell division. In addition to demonstrating metabolic requirements for reproductive development, this work also has implications for understanding the mechanisms behind therapeutic interventions that target NAD(+) salvage biosynthesis for the purposes of inhibiting tumor growth.
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