Ribbon constrains dendritic pruning via actin scaffolding and exocyst complex.

Wanting Wang, Su Wang, Yuhao Yuan, Menglong Rui

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Article in Cellular & molecular biology letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 authors.

Wanting Wang *School of Life Science and Technology, the Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing, China.

Su Wang *School of Life Science and Technology, the Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing, China.

Yuhao YuanSchool of Life Science and Technology, the Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing, China.

Menglong RuiSchool of Life Science and Technology, the Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing, China. ruimenglong@seu.edu.cn.

Funding

Fundamental Research Funds for the Central Universities 2242024RCB0031National Natural Science Foundation of China 32100784Natural Science Foundation of Jiangsu Province BK20221458

6 · The paper itself

Abstract

backgroundDuring animal development, neurons selectively remove superfluous synaptic connections, strengthen key synapses, and optimize neural circuits in the brain, which is a core mechanism for fine-tuning the development of the nervous system. Drosophila class IV dendritic arborization (C4da) sensory neurons undergo dendrite-specific pruning during development. Nevertheless, the cell-autonomous inhibitory mechanisms of dendritic pruning in C4da neurons are largely unknown. METHODS AND

resultsHere, we discovered Ribbon (Rib), a nuclear BTB-domain protein, whose malfunction in C4da neurons causes a precocious occurrence of dendritic pruning. Our study further shows that the regulation of dendritic pruning by Rib is dependent on Akt/Tor signaling. Moreover, actin polymerization factors and exocyst complex subunits are also involved in repressing dendritic pruning and function as downstream effectors of Rib and Akt/Tor signaling.

conclusionsOverall, the present study reveals a cell-autonomous inhibitory mechanism of Rib in dendritic pruning, with a perspective to provide new insights into neurodevelopment and the pathogenesis of relevant neurological disorders.

Indexed as

ActinsDendritesDrosophila melanogasterDrosophila ProteinsNeuronal PlasticityAnimalsNeurodevelopmentProto-Oncogene Proteins c-aktSensory Receptor CellsSignal TransductionTOR Serine-Threonine KinasesActinsDrosophila ProteinsProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesActin scaffoldingAkt/Tor signalingExocyst complexNeurite pruningRibbon

Identifiers

PMID41928094

DOI10.1186/s11658-026-00903-1

PMCPMC13169544

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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.