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

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 don't 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,

SUBMITTER: Qu Z 

PROVIDER: S-EPMC12668009 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature