ArticleThe Journal of biological chemistry2009
Caenorhabditits elegans LRK-1 and PINK-1 act antagonistically in stress response and neurite outgrowth.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 1 of them a synthesis that pooled it.
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Who cites it
99 citing papers in PubMed, 1 synthesis or guideline pooled it, 191 citations in OpenAlex.
- Competing endogenous RNA (ceRNA) networks in Parkinson's disease: A systematic review.Frontiers in cellular neuroscience · 2023Pooled it
- Box C/D snoRNPs and MDT-15/MED15 regulate mitochondrial surveillance and mitophagy via fatty acid metabolism.GeroScience · 2026Article
- Programmed mitophagy at the oocyte-to-zygote transition promotes lineage endurance.Nature cell biology · 2026Article
- Unraveling Molecular Targets for Neurodegenerative Diseases ThroughInternational journal of molecular sciences · 2025Review
- Mitochondrial Quality Control in Alzheimer's Disease: Insights fromAntioxidants (Basel, Switzerland) · 2024Review
- LRRK2 Gly2019Ser Mutation Promotes ER Stress via Interacting with THBS1/TGF-β1 in Parkinson's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Review
- The joint effects of nanoplastics and TBBPA on neurodevelopmental toxicity inToxicology research · 2023Article
- Endogenous PTEN-Induced Kinase 1 Regulates Dendritic Architecture and Spinogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- The parkinsonian LRRK2 R1441G mutation shows macroautophagy-mitophagy dysregulation concomitant with endoplasmic reticulum stress.Cell biology and toxicology · 2022Article
- Review
- Oocyte mitophagy is critical for extended reproductive longevity.PLoS genetics · 2022Article
- Article
- Significant modulations of linc001128 and linc0938 with miR-24-3p and miR-30c-5p in Parkinson disease.Scientific reports · 2022Article
- Animal models in the study of Alzheimer's disease and Parkinson's disease: A historical perspective.Animal models and experimental medicine · 2022Review
- Modelling the functional genomics of Parkinson's disease in Caenorhabditis elegans: LRRK2 and beyond.Bioscience reports · 2021Review
- Mitochondria-affecting small molecules ameliorate proteostasis defects associated with neurodegenerative diseases.Scientific reports · 2021Article
- Animal Models of Autosomal Recessive Parkinsonism.Biomedicines · 2021Review
- Small heterodimer partner (SHP) aggravates ER stress in Parkinson's disease-linked LRRK2 mutant astrocyte by regulating XBP1 SUMOylation.Journal of biomedical science · 2021Article
- Complex pleiotropic genetic architecture of evolved heat stress and oxidative stress resistance in the nematode Caenorhabditis remanei.G3 (Bethesda, Md.) · 2021Article
39 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in two genes encoding the putative kinases LRRK2 and PINK1 have been associated with inherited variants of Parkinson disease. The physiological role of both proteins is not known at present, but studies in model organisms have linked their mutants to distinct aspects of mitochondrial dysfunction, increased vulnerability to oxidative and endoplasmic reticulum stress, and intracellular protein sorting. Here, we show that a mutation in the Caenorhabditits elegans homologue of the PTEN-induced kinase pink-1 gene resulted in reduced mitochondrial cristae length and increased paraquat sensitivity of the nematode. Moreover, the mutants also displayed defects in axonal outgrowth of a pair of canal-associated neurons. We demonstrate that in the absence of lrk-1, the C. elegans homologue of human LRRK2, all phenotypic aspects of pink-1 loss-of-function mutants were suppressed. Conversely, the hypersensitivity of lrk-1 mutant animals to the endoplasmic reticulum stressor tunicamycin was reduced in a pink-1 mutant background. These results provide the first evidence of an antagonistic role of PINK-1 and LRK-1. Due to the similarity of the C. elegans proteins to human LRRK2 and PINK1, we suggest a common role of both factors in cellular functions including stress response and regulation of neurite outgrowth. This study might help to link pink-1/PINK1 and lrk-1/LRRK2 function to the pathological processes resulting from Parkinson disease-related mutants in both genes, the first manifestations of which are cytoskeletal defects in affected neurons.
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