ArticleThe Journal of cell biology2015
Rab8, POSH, and TAK1 regulate synaptic growth in a Drosophila model of frontotemporal dementia.
Article in The Journal of cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 88 citations in OpenAlex.
- The Ku80-p53-SIRT1 axis in DNA damage response contributes to sporadic and familial ALS and FTD.Nature communications · 2025Article
- A force-sensitive mutation reveals a non-canonical role for dynein in anaphase progression.The Journal of cell biology · 2024Article
- Identification of common biomarkers in diabetic kidney disease and cognitive dysfunction using machine learning algorithms.Scientific reports · 2024Article
- ESCRT disruption provides evidence against trans-synaptic signaling via extracellular vesicles.The Journal of cell biology · 2024Article
- Synaptopathy: presynaptic convergence in frontotemporal dementia and amyotrophic lateral sclerosis.Brain : a journal of neurology · 2024Review
- ESCRT disruption provides evidence against transsynaptic signaling functions for extracellular vesicles.bioRxiv : the preprint server for biology · 2024Article
- Identification of secretory autophagy as a mechanism modulating activity-induced synaptic remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- tsCRISPR based identification of Rab proteins required for the recycling ofFrontiers in cell and developmental biology · 2024Article
- The endolysosomal pathway and ALS/FTD.Trends in neurosciences · 2023Review
- Senataxin helicase, the causal gene defect in ALS4, is a significant modifier of C9orf72 ALS G4C2 and arginine-containing dipeptide repeat toxicity.Acta neuropathologica communications · 2023Article
- Non-muscle MYH10/myosin IIB recruits ESCRT-III to participate in autophagosome closure to maintain neuronal homeostasis.Autophagy · 2023Article
- An AP-3-dependent pathway directs phagosome fusion with Rab8 and Rab11 vesicles involved in TLR2 signaling.Traffic (Copenhagen, Denmark) · 2022Article
- The enhanced association between mutant CHMP2B and spastin is a novel pathological link between frontotemporal dementia and hereditary spastic paraplegias.Acta neuropathologica communications · 2022Article
- Local regulation of extracellular vesicle traffic by the synaptic endocytic machinery.The Journal of cell biology · 2022Article
- The Putative Drosophila TMEM184B Ortholog Tmep Ensures Proper Locomotion by Restraining Ectopic Firing at the Neuromuscular Junction.Molecular neurobiology · 2022Article
- Wnt5a protects motor neurons in amyotrophic lateral sclerosis by regulating the Wnt/CaAmerican journal of translational research · 2022Article
- C9orf72 ALS-FTD: recent evidence for dysregulation of the autophagy-lysosome pathway at multiple levels.Autophagy · 2021Review
- Opposing functions for retromer and Rab11 in extracellular vesicle traffic at presynaptic terminals.The Journal of cell biology · 2021Article
- Presynaptic accumulation of α-synuclein causes synaptopathy and progressive neurodegeneration inBrain communications · 2021Article
- Multiple Pathways of LRRK2-G2019S/Rab10 Interaction in Dopaminergic Neurons.Journal of Parkinson's disease · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Mutations in genes essential for protein homeostasis have been identified in frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) patients. Why mature neurons should be particularly sensitive to such perturbations is unclear. We identified mutations in Rab8 in a genetic screen for enhancement of an FTD phenotype associated with ESCRT-III dysfunction. Examination of Rab8 mutants or motor neurons expressing a mutant ESCRT-III subunit, CHMP2B(Intron5), at the Drosophila melanogaster neuromuscular junction synapse revealed synaptic overgrowth and endosomal dysfunction. Expression of Rab8 rescued overgrowth phenotypes generated by CHMP2B(Intron5). In Rab8 mutant synapses, c-Jun N-terminal kinase (JNK)/activator protein-1 and TGF-β signaling were overactivated and acted synergistically to potentiate synaptic growth. We identify novel roles for endosomal JNK-scaffold POSH (Plenty-of-SH3s) and a JNK kinase kinase, TAK1, in regulating growth activation in Rab8 mutants. Our data uncover Rab8, POSH, and TAK1 as regulators of synaptic growth responses and point to recycling endosome as a key compartment for synaptic growth regulation during neurodegenerative processes.
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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.