ArticleDevelopment (Cambridge, England)2009
Nicotinamidase modulation of NAD+ biosynthesis and nicotinamide levels separately affect reproductive development and cell survival in C. elegans.
Article in Development (Cambridge, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
38 citing papers in PubMed, 47 citations in OpenAlex.
- Insulin and epidermal signals independently shape sexually dimorphic neurite branching in C. elegans.EMBO reports · 2025Article
- De novo NADCommunications biology · 2025Article
- Argonaute CSR-1A promotes H3K9me3 maintenance to protect somatic development in offspring.Nucleic acids research · 2025Article
- Supplementation with NAD+ and its precursors: A rescue of female reproductive diseases.Biochemistry and biophysics reports · 2024Review
- DMHCell metabolism · 2024Article
- A link between energy metabolism and plant host adaptation states in the two-spotted spider mite, Tetranychus urticae (Koch).Scientific reports · 2023Article
- An insecticide target in mechanoreceptor neurons.Science advances · 2022Article
- Noncanonical necrosis in 2 different cell types in a Caenorhabditis elegans NAD+ salvage pathway mutant.G3 (Bethesda, Md.) · 2022Article
- Caenorhabditis elegans as a model for studies on quinolinic acid-induced NMDAR-dependent glutamatergic disorders.Brain research bulletin · 2021Article
- NADCell reports · 2021Article
- Overactive EGF signaling suppresses amicroPublication biology · 2021Article
- Overactive EGF signaling promotes uv1 cell survivalmicroPublication biology · 2020Article
- Genetic and functional diversification of chemosensory pathway receptors in mosquito-borne filarial nematodes.PLoS biology · 2020Article
- Inhibition of the NAD salvage pathway in schistosomes impairs metabolism, reproduction, and parasite survival.PLoS pathogens · 2020Article
- Purine Homeostasis Is Necessary for Developmental Timing, Germline Maintenance and Muscle Integrity inGenetics · 2019Article
- Cytoplasmic and Mitochondrial NADPH-Coupled Redox Systems in the Regulation of Aging.Nutrients · 2019Review
- Expanded genetic screening ineLife · 2018Article
- Non-Mendelian assortment of homologous autosomes of different sizes in males is the ancestral state in the Caenorhabditis lineage.Scientific reports · 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
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Nicotinamide adenine dinucleotide (NAD(+)) is a central molecule in cellular metabolism and an obligate co-substrate for NAD(+)-consuming enzymes, which regulate key biological processes such as longevity and stress responses. Although NAD(+) biosynthesis has been intensely studied, little analysis has been done in developmental models. We have uncovered novel developmental roles for a nicotinamidase (PNC), the first enzyme in the NAD(+) salvage pathway of invertebrates. Mutations in the Caenorhabditis elegans nicotinamidase PNC-1 cause developmental and functional defects in the reproductive system; the development of the gonad is delayed, four uterine cells die by necrosis and the mutant animals are egg-laying defective. The temporal delay in gonad development results from depletion of the salvage pathway product NAD(+), whereas the uv1 cell necrosis and egg-laying defects result from accumulation of the substrate nicotinamide. Thus, regulation of both substrate and product level is key to the biological activity of PNC-1. We also find that diet probably affects the levels of these metabolites, as it affects phenotypes. Finally, we identified a secreted isoform of PNC-1 and confirmed its extracellular localization and functional activity in vivo. We demonstrate that nicotinamide phosphoribosyltransferase (Nampt), the equivalent enzyme in nicotinamide recycling to NAD(+) in vertebrates, can functionally substitute for PNC-1. As Nampt is also secreted, we postulate an evolutionarily conserved extracellular role for NAD(+) biosynthetic enzymes during development and physiology.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.