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May 2, 2026Journal of Biological Chemistry0 citationsOpen Access

Kif15 Orchestrates Neuronal-Microglial Communication via CX3CL1 to Impede Nerve Regeneration

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RWRonghua WuWZWei ZhangXQXiaowei Qian

Key Points

  • This study aims to investigate the role of Kif15 in neuronal-microglial communication and its impact on nerve regeneration after injury.
  • Kif15 knockout mice were analyzed for functional recovery following sciatic nerve injury.
  • Single-nucleus RNA sequencing (snRNA-seq) was performed on spinal cord tissues to assess gene expression profiles.
  • Molecular analysis evaluated the expression and localization of neuronal CX3CL1 and its interaction with microglial CX3CR1.
  • Kif15 KO mice showed accelerated functional recovery after sciatic nerve injury compared to wild-type mice.
  • Differential gene expression in Kif15 KO mice indicated a neuroprotective shift in neurons and a repair-promoting profile in microglia.
  • Downregulation of the CX3CL1-CX3CR1 signaling pathway was observed in Kif15 KO mice, affecting neuronal-microglial communication.

Abstract

Kinesins, a class of microtubule (MT)-dependent molecular motors, regulate MT dynamics and MT-mediated transport. We previously identified Kif15 (kinesin-12) as a key player in axonal growth by modulating MT remodeling during neuronal development, and more recently, its involvement in protein localization. In this study, we observed that Kif15 knockout (Kif15 KO) mice exhibited accelerated functional recovery after sciatic nerve injury. To investigate the cellular responses underlying this enhanced recovery after axotomy, spinal cord tissues from the injured regions were collected for single-nucleus RNA sequencing (snRNA-seq). The snRNA-seq results revealed differential genes expression in neurons, indicating a neuroprotective shift in Kif15 KO mice, and in microglia, where a repair-promoting and synapse-modulating profile was observed. Notably, the CX3CL1-CX3CR1 signaling pathway, critical for neuronal-microglial communication, was downregulated in Kif15 KO mice compared to wild-type controls. Further molecular analysis indicated that Kif15 facilitated the expression and localization of neuronal CX3CL1, which, in turn, influenced microglial function via the receptor CX3CR1. Our findings highlight a novel role for Kif15 in regulating neuronal-microglial communication through modulation of CX3CL1 signaling.

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Cite This Study

Wu et al. (2026) studied this question.

synapsesocial.com/papers/69f5939871405d493affea9dhttps://doi.org/10.1016/j.jbc.2026.113090
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