Injury-induced nuclear export of RNA-binding proteins drives mRNA stabilization and translation to promote dendrite regeneration

Qu, Z.; Yan, D.

doi:10.1101/2025.11.18.688889

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bioRxiv · 10.1101/2025.11.18.688889

Injury-induced nuclear export of RNA-binding proteins drives mRNA stabilization and translation to promote dendrite regeneration

Qu, Z.·Yan, D.

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Abstract

Dendrite regeneration is critical for restoring neuronal connectivity after injury, yet the underlying molecular mechanisms remain poorly understood. Using C. elegans as a model and through a forward genetic screen, we identified the conserved insulin degrading enzyme idr-1 and the RNA-binding protein rbm-42 as key regulators of dendrite regeneration, where idr-1 functions upstream of rbm-42. We further show that ced-7, one of the core components of the phagocytosis pathway, acting down stream of rbm-42, while other components of this pathway dont play significant roles in dendrite regeneration. In addition, we demonstrate that upon injury IDR-1 can promote RBM-42 nuclear export following injury, enabling its dendritic localization. RBM-42, in turn, promotes the translation of ced-7 and facilitates microtubule assembly. In conclusion, our findings define a novel conserved signaling cascade coupling injury-induced nuclear export of RNA binding proteins to local regulation and dendrite regeneration, providing new mechanistic insight into neuronal repair.

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Qu, Z., Yan, D.. 2025-11-18. Injury-induced nuclear export of RNA-binding proteins drives mRNA stabilization and translation to promote dendrite regeneration. https://doi.org/10.1101/2025.11.18.688889

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