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Background <p>During 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. <i>Drosophila</i> 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.</p> Methods and results <p>Here, 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.</p> Conclusions <p>Overall, 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.</p>

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Ribbon constrains dendritic pruning via actin scaffolding and exocyst complex

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月2日

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  • Wanting Wang,
  • Su Wang,
  • Yuhao Yuan,
  • Menglong Rui

摘要

Background

During 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 results

Here, 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.

Conclusions

Overall, 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.