Kinesin family member 2A gates nociception

Swagata Dey, Omer Barkai, Irena Gokhman, Sapir Suissa, Rebecca Haffner-Krausz, Noa Wigoda, Ester Feldmesser, Shifra Ben-Dor, Andrew Kovalenko, Alexander Binshtok, Avraham Yaron*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Nociceptive axons undergo remodeling as they innervate their targets during development and in response to environmental insults and pathological conditions. How is nociceptive morphogenesis regulated? Here, we show that the microtubule destabilizer kinesin family member 2A (Kif2a) is a key regulator of nociceptive terminal structures and pain sensitivity. Ablation of Kif2a in sensory neurons causes hyperinnervation and hypersensitivity to noxious stimuli in young adult mice, whereas touch sensitivity and proprioception remain unaffected. Computational modeling predicts that structural remodeling is sufficient to explain the phenotypes. Furthermore, Kif2a deficiency triggers a transcriptional response comprising sustained upregulation of injury-related genes and homeostatic downregulation of highly specific channels and receptors at the late stage. The latter effect can be predicted to relieve the hyperexcitability of nociceptive neurons, despite persisting morphological aberrations, and indeed correlates with the resolution of pain hypersensitivity. Overall, we reveal a critical control node defining nociceptive terminal structure, which is regulating nociception.

Original languageAmerican English
Article number113257
JournalCell Reports
Issue number10
StatePublished - 31 Oct 2023

Bibliographical note

Publisher Copyright:
© 2023 The Author(s)


  • CP: Neuroscience
  • Kif2a
  • axonal degeneration
  • microtubules
  • nociception


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