ArticlePLoS biology2019
A hormone receptor pathway cell-autonomously delays neuron morphological aging by suppressing endocytosis.
Article in PLoS biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- NDR kinase SAX-1 controls dendrite branch-specific elimination during neuronal remodeling in C. elegans.The EMBO journal · 2026Article
- Cell-intrinsic mTOR/LET-363 influences morphological aging of the ALM touch receptor neuron in Caenorhabditis elegans.PloS one · 2026Article
- Review
- Expansion of lysosomal capacity in early adult neurons driven by TFEB/HLH-30 protects dendrite maintenance during aging in Caenorhabditis elegans.PLoS biology · 2025Article
- Dendrite morphogenesis in Caenorhabditis elegans.Genetics · 2024Review
- EGFR signal transduction is downregulated in C. elegans vulval precursor cells during dauer diapause.Development (Cambridge, England) · 2022Article
- Article
- CRMP/UNC-33 organizes microtubule bundles for KIF5-mediated mitochondrial distribution to axon.PLoS genetics · 2021Article
- Starvation Responses Throughout theGenetics · 2020Review
- Mutually exclusive dendritic arbors in C. elegans neurons share a common architecture and convergent molecular cues.PLoS genetics · 2020Article
- FOXO Regulates Neuromuscular Junction Homeostasis DuringFrontiers in aging neuroscience · 2020Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Neurons have a lifespan that parallels that of the organism and are largely irreplaceable. Their unusually long lifespan predisposes neurons to neurodegenerative disease. We sought to identify physiological mechanisms that delay neuron aging in Caenorhabditis elegans by asking how neuron morphological aging is arrested in the long-lived, alternate organismal state, the dauer diapause. We find that a hormone signaling pathway, the abnormal DAuer Formation (DAF) 12 nuclear hormone receptor (NHR) pathway, functions cell-intrinsically in the dauer diapause to arrest neuron morphological aging, and that same pathway can be cell-autonomously manipulated during normal organismal aging to delay neuron morphological aging. This delayed aging is mediated by suppressing constitutive endocytosis, which alters the subcellular localization of the actin regulator T cell lymphoma Invasion And Metastasis 1 (TIAM-1), thereby decreasing age-dependent neurite growth. Intriguingly, we show that suppressed endocytosis appears to be a general feature of cells in diapause, suggestive that this may be a mechanism to halt the growth and other age-related programs supported by most endosome recycling.
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Registered trials
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.