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ATF4 selectively regulates heat nociception and contributes to kinesin-mediated TRPM3 trafficking

Author

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  • Man-Xiu Xie

    (Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine)

  • Xian-Ying Cao

    (Hainan University
    State Key Laboratory of Marine Resources Utilization of South China Sea)

  • Wei-An Zeng

    (Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine)

  • Ren-Chun Lai

    (Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine)

  • Lan Guo

    (Hainan University)

  • Jun-Chao Wang

    (Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine)

  • Yi-Bin Xiao

    (Zhongshan School of Medicine of Sun Yat-sen University)

  • Xi Zhang

    (Zhongshan School of Medicine of Sun Yat-sen University)

  • Di Chen

    (Hainan University)

  • Xian-Guo Liu

    (Zhongshan School of Medicine of Sun Yat-sen University)

  • Xiao-Long Zhang

    (Guangdong Academy of Medical Sciences)

Abstract

Effective treatments for patients suffering from heat hypersensitivity are lacking, mostly due to our limited understanding of the pathogenic mechanisms underlying this disorder. In the nervous system, activating transcription factor 4 (ATF4) is involved in the regulation of synaptic plasticity and memory formation. Here, we show that ATF4 plays an important role in heat nociception. Indeed, loss of ATF4 in mouse dorsal root ganglion (DRG) neurons selectively impairs heat sensitivity. Mechanistically, we show that ATF4 interacts with transient receptor potential cation channel subfamily M member-3 (TRPM3) and mediates the membrane trafficking of TRPM3 in DRG neurons in response to heat. Loss of ATF4 also significantly decreases the current and KIF17-mediated trafficking of TRPM3, suggesting that the KIF17/ATF4/TRPM3 complex is required for the neuronal response to heat stimuli. Our findings unveil the non-transcriptional role of ATF4 in the response to heat stimuli in DRG neurons.

Suggested Citation

  • Man-Xiu Xie & Xian-Ying Cao & Wei-An Zeng & Ren-Chun Lai & Lan Guo & Jun-Chao Wang & Yi-Bin Xiao & Xi Zhang & Di Chen & Xian-Guo Liu & Xiao-Long Zhang, 2021. "ATF4 selectively regulates heat nociception and contributes to kinesin-mediated TRPM3 trafficking," Nature Communications, Nature, vol. 12(1), pages 1-18, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-21731-1
    DOI: 10.1038/s41467-021-21731-1
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