ArticleProceedings of the National Academy of Sciences of the United States of America2006
wasted away, a Drosophila mutation in triosephosphate isomerase, causes paralysis, neurodegeneration, and early death.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. 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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Who cites it
38 citing papers in PubMed, 71 citations in OpenAlex.
- Molecular Transducers of Human Skeletal Muscle Remodeling under Different Loading States.Cell reports · 2020Trial
- The Remarkable Role of Triosephosphate Isomerase in Diabetes Pathophysiology.International journal of molecular sciences · 2025Review
- Molecular Adjustment to a Social Niche: Brain Transcriptomes Reveal Divergent Influence of Social Environment on the Two Queen Morphs of the Ant Temnothorax rugatulus.Molecular ecology · 2025Article
- Methylglyoxal-Induced Modifications in Human Triosephosphate Isomerase: Structural and Functional Repercussions of Specific Mutations.Molecules (Basel, Switzerland) · 2024Article
- Triose-phosphate isomerase deficiency is associated with a dysregulation of synaptic vesicle recycling inFrontiers in synaptic neuroscience · 2023Article
- Low catalytic activity is insufficient to induce disease pathology in triosephosphate isomerase deficiency.Journal of inherited metabolic disease · 2019Article
- Missense variant in TPI1 (Arg189Gln) causes neurologic deficits through structural changes in the triosephosphate isomerase catalytic site and reduced enzyme levels in vivo.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- Review
- The Role of Advanced Glycation End Products in Aging and Metabolic Diseases: Bridging Association and Causality.Cell metabolism · 2018Review
- Pathways to neurodegeneration: lessons learnt from unbiased genetic screens inJournal of genetics · 2018Review
- Article
- Proteome changes in the agingInternational journal of mass spectrometry · 2018Article
- Structural and Genetic Studies Demonstrate Neurologic Dysfunction in Triosephosphate Isomerase Deficiency Is Associated with Impaired Synaptic Vesicle Dynamics.PLoS genetics · 2016Article
- Structural Basis for Redox Regulation of Cytoplasmic and Chloroplastic Triosephosphate Isomerases fromFrontiers in plant science · 2016Article
- Death following traumatic brain injury in Drosophila is associated with intestinal barrier dysfunction.eLife · 2015Article
- A neuroprotective function of NSF1 sustains autophagy and lysosomal trafficking in Drosophila.Genetics · 2015Article
- Triosephosphate isomerase I170V alters catalytic site, enhances stability and induces pathology in a Drosophila model of TPI deficiency.Biochimica et biophysica acta · 2015Article
- SDHAF4 promotes mitochondrial succinate dehydrogenase activity and prevents neurodegeneration.Cell metabolism · 2014Article
- Evidence of a triosephosphate isomerase non-catalytic function crucial to behavior and longevity.Journal of cell science · 2013Article
- Early mitochondrial dysfunction leads to altered redox chemistry underlying pathogenesis of TPI deficiency.Neurobiology of disease · 2013Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
To identify genes required for maintaining neuronal viability, we screened our collection of Drosophila temperature-sensitive paralytic mutants for those exhibiting shortened lifespan and neurodegeneration. Here, we describe the characterization of wasted away (wstd), a recessive, hypomorphic mutation that causes progressive motor impairment, vacuolar neuropathology, and severely reduced lifespan. We demonstrate that the affected gene encodes the glycolytic enzyme, triosephosphate isomerase (Tpi). Mutations causing Tpi deficiency in humans are also characterized by progressive neurological dysfunction, neurodegeneration, and early death. In Tpi-deficient flies and humans, a decrease in ATP levels did not appear to cause the observed phenotypes because ATP levels remained normal. We also found no genetic evidence that the mutant Drosophila Tpi was misfolded or involved in aberrant protein-protein associations. Instead, we favor the hypothesis that mutations in Tpi lead to an accumulation of methylglyoxal and the consequent enhanced production of advanced glycation end products, which are ultimately responsible for the death and dysfunction of Tpi-deficient neurons. Our results highlight an essential protective role of Tpi and support the idea that advanced glycation end products may also contribute to pathogenesis of other neurological disorders.
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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.