ArticleThe Journal of biological chemistry2008
The Caenorhabditis elegans K10C2.4 gene encodes a member of the fumarylacetoacetate hydrolase family: a Caenorhabditis elegans model of type I tyrosinemia.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 37 citations in OpenAlex.
- Fumarylacetoacetate Hydrolase Regulates Seed Dormancy and Germination Through the Gibberellin Pathway in Arabidopsis.Plants (Basel, Switzerland) · 2025Article
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- Isolation, profiling, and tracking of extracellular vesicle cargo in Caenorhabditis elegans.Current biology : CB · 2022Article
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- Beyond Proteostasis: Lipid Metabolism as a New Player in ER Homeostasis.Metabolites · 2021Review
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- Sugar suppresses cell death caused by disruption of fumarylacetoacetate hydrolase in Arabidopsis.Planta · 2016Article
- LC-MS proteomics analysis of the insulin/IGF-1-deficient Caenorhabditis elegans daf-2(e1370) mutant reveals extensive restructuring of intermediary metabolism.Journal of proteome research · 2014Article
- Oxidative stress in aging: advances in proteomic approaches.Oxidative medicine and cellular longevity · 2014Review
- Disruption of fumarylacetoacetate hydrolase causes spontaneous cell death under short-day conditions in Arabidopsis.Plant physiology · 2013Article
- TATN-1 mutations reveal a novel role for tyrosine as a metabolic signal that influences developmental decisions and longevity in Caenorhabditis elegans.PLoS genetics · 2013Article
- Improved vectors for selection of transgenic Caenorhabditis elegans.Methods in molecular biology (Clifton, N.J.) · 2013Article
- Novel structural arrangement of nematode cystathionine β-synthases: characterization of Caenorhabditis elegans CBS-1.The Biochemical journal · 2012Article
- Relationship of electrophilic stress to aging.Free radical biology & medicine · 2011Review
- The garlic constituent diallyl trisulfide increases the lifespan of C. elegans via skn-1 activation.Experimental gerontology · 2011Article
- Biology of the Mi-2/NuRD Complex in SLAC (Stemness, Longevity/Ageing, and Cancer).Gene regulation and systems biology · 2011Article
- The production of C. elegans transgenes via recombineering with the galK selectable marker.Journal of visualized experiments : JoVE · 2011Article
- RNAi screening implicates a SKN-1-dependent transcriptional response in stress resistance and longevity deriving from translation inhibition.PLoS genetics · 2010Article
- skn-1-Dependent and -independent regulation of aip-1 expression following metabolic stress in Caenorhabditis elegans.Molecular and cellular biology · 2010Article
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4 authors at 2 institutions in 1 country.
Funding
Abstract
In eukaryotes and many bacteria, tyrosine is degraded to produce energy via a five-step tyrosine degradation pathway. Mutations affecting the tyrosine degradation pathway are also of medical importance as mutations affecting enzymes in the pathway are responsible for type I, type II, and type III tyrosinemia. The most severe of these is type I tyrosinemia, which is caused by mutations affecting the last enzyme in the pathway, fumarylacetoacetate hydrolase (FAH). So far, tyrosine degradation in the nematode Caenorhabditis elegans has not been studied; however, genes predicted to encode enzymes in this pathway have been identified in several microarray, proteomic, and RNA interference (RNAi) screens as perhaps being involved in aging and the control of protein folding. We sought to identify and characterize the genes in the worm tyrosine degradation pathway as an initial step in understanding these findings. Here we describe the characterization of the K10C2.4, which encodes a homolog of FAH. RNAi directed against K10C2.4 produces a lethal phenotype consisting of death in young adulthood, extensive damage to the intestine, impaired fertility, and activation of oxidative stress and endoplasmic stress response pathways. This phenotype is due to alterations in tyrosine metabolism as increases in dietary tyrosine enhance it, and inhibition of upstream enzymes in tyrosine degradation with RNAi or genetic mutations reduces the phenotype. We also use our model to identify genes that suppress the damage produced by K10C2.4 RNAi in a pilot genetic screen. Our results establish worms as a model for the study of type I tyrosinemia.
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