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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Sweeney, Sean T. Lu, Yubing West, Ryan J. H. Gao, Fen-biao Marie, Bruno |
| Description | Author Affiliation: West RJ ( Department of Biology and Hull York Medical School, University of York, Heslington, York YO10 5DD, England, UK Department of Biology and Hull York Medical School, University of York, Heslington, York YO10 5DD, England, UK.); Lu Y ( Department of Neurology, University of Massachusetts Medical School, Worcester, MA 01605.); Marie B ( Institute of Neurobiology, Medical Sciences Campus, University of Puerto Rico, San Juan, Puerto Rico 00901.); Gao FB ( Department of Neurology, University of Massachusetts Medical School, Worcester, MA 01605.); Sweeney ST ( Department of Biology and Hull York Medical School, University of York, Heslington, York YO10 5DD, England, UK Department of Biology and Hull York Medical School, University of York, Heslington, York YO10 5DD, England, UK sean.sweeney@york.ac.uk.) |
| 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. |
| ISSN | 00219525 |
| e-ISSN | 15408140 |
| Journal | The Journal of Cell Biology |
| Issue Number | 7 |
| Volume Number | 208 |
| Language | English |
| Publisher | Rockefeller University Press (United States) |
| Publisher Date | 2015-03-30 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Carrier Proteins Genetics Cytoskeletal Proteins Drosophila Proteins Drosophila Melanogaster Metabolism Frontotemporal Dementia GTP Phosphohydrolases MAP Kinase Kinase Kinases Nerve Tissue Proteins Animals Animals, Genetically Modified Cells, Cultured Disease Models, Animal Endosomal Sorting Complexes Required For Transport Endosomes JNK Mitogen-Activated Protein Kinases Mice Mice, Inbred C57BL Mutation Neuromuscular Junction Pathology Signal Transduction Transcription Factor AP-1 Transforming Growth Factor Beta Vesicular Transport Proteins Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Cell Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Medicine |
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