Yuting Liu, Vinicius N Duarte, Katherine L Thompson-Peer
{"title":"Late endosome trafficking is slower in regenerated dendrites.","authors":"Yuting Liu, Vinicius N Duarte, Katherine L Thompson-Peer","doi":"10.1159/dne/aclag007","DOIUrl":null,"url":null,"abstract":"<p><p>Organelle trafficking is essential for neuronal function and homeostasis, particularly in dendrites where transport is required to maintain complex arbors. Following dendritic injury, extensive cellular reorganization occurs during regeneration, yet how this remodeling affects organelle transport dynamics remains poorly understood. To assess the consequences of regeneration on dendritic trafficking, we examined Rab7-labeled late endosome (LE) movement in class IV dendritic arborization neurons of Drosophila after dendrite injury. Using quantitative live imaging analysis, we found that retrograde LE trafficking speed is significantly reduced in regenerated dendrites compared to uninjured controls. However, anterograde LE trafficking speed, the directional bias of LE movement, the proportion of motile versus stationary organelles, LE number, and run length were not significantly different between uninjured versus regenerated neurons at either time point examined. These findings demonstrate that dendritic regeneration selectively impairs retrograde transport kinetics while preserving anterograde transport and directional control mechanisms. Regenerated dendrites are thinner than uninjured controls at early stages of regrowth but recover to normal caliber by later stages, yet retrograde transport deficits persist, suggesting caliber-independent regulation of retrograde transport speed. Our results suggest that altered organelle trafficking dynamics may represent a fundamental consequence of neuronal injury responses, with potential implications for understanding transport defects in regeneration after injury or disease involving dendritic damage.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"1"},"PeriodicalIF":2.1000,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Developmental Neuroscience","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1159/dne/aclag007","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"DEVELOPMENTAL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Organelle trafficking is essential for neuronal function and homeostasis, particularly in dendrites where transport is required to maintain complex arbors. Following dendritic injury, extensive cellular reorganization occurs during regeneration, yet how this remodeling affects organelle transport dynamics remains poorly understood. To assess the consequences of regeneration on dendritic trafficking, we examined Rab7-labeled late endosome (LE) movement in class IV dendritic arborization neurons of Drosophila after dendrite injury. Using quantitative live imaging analysis, we found that retrograde LE trafficking speed is significantly reduced in regenerated dendrites compared to uninjured controls. However, anterograde LE trafficking speed, the directional bias of LE movement, the proportion of motile versus stationary organelles, LE number, and run length were not significantly different between uninjured versus regenerated neurons at either time point examined. These findings demonstrate that dendritic regeneration selectively impairs retrograde transport kinetics while preserving anterograde transport and directional control mechanisms. Regenerated dendrites are thinner than uninjured controls at early stages of regrowth but recover to normal caliber by later stages, yet retrograde transport deficits persist, suggesting caliber-independent regulation of retrograde transport speed. Our results suggest that altered organelle trafficking dynamics may represent a fundamental consequence of neuronal injury responses, with potential implications for understanding transport defects in regeneration after injury or disease involving dendritic damage.
期刊介绍:
''Developmental Neuroscience'' is a multidisciplinary journal publishing papers covering all stages of invertebrate, vertebrate and human brain development. Emphasis is placed on publishing fundamental as well as translational studies that contribute to our understanding of mechanisms of normal development as well as genetic and environmental causes of abnormal brain development. The journal thus provides valuable information for both physicians and biologists. To meet the rapidly expanding information needs of its readers, the journal combines original papers that report on progress and advances in developmental neuroscience with concise mini-reviews that provide a timely overview of key topics, new insights and ongoing controversies. The editorial standards of ''Developmental Neuroscience'' are high. We are committed to publishing only high quality, complete papers that make significant contributions to the field.