2. Academic Validation
  3. mTOR mutation disrupts larval zebrafish tail fin regeneration via regulating proliferation of blastema cells and mitochondrial functions

mTOR mutation disrupts larval zebrafish tail fin regeneration via regulating proliferation of blastema cells and mitochondrial functions

  • J Orthop Surg Res. 2024 May 29;19(1):321. doi: 10.1186/s13018-024-04802-z.
Gongyi Xiao 1,  Xiangwei Li 1,  Huiping Yang 2,  Ruobin Zhang 3,  Junlan Huang 3,  Yu Tian 3 4,  Mao Nie 5,  Xianding Sun 6
Affiliations

Affiliations

  • 1 Center for Joint Surgery, Department of Orthopedic Surgery, The Second Affiliated Hospital of Chongqing Medical University, 74 Linjiang Road, Chongqing, 400010, China.
  • 2 Department of Cardiology, The Second Affiliated Hospital of Chongqing Medical University, 74 Linjiang Road, Chongqing, 400010, China.
  • 3 Department of Wound Repair and Rehabilitation Medicine, State Key Laboratory of Trauma, Burns and Combined Injury, Trauma Center, Research Institute of Surgery, Daping Hospital, Army Medical University, Chongqing, 400042, China.
  • 4 Ministry of Education College of Bioengineering, Chongqing University, Chongqing, 400044, P. R. China.
  • 5 Center for Joint Surgery, Department of Orthopedic Surgery, The Second Affiliated Hospital of Chongqing Medical University, 74 Linjiang Road, Chongqing, 400010, China. 302218@cqmu.edu.cn.
  • 6 Center for Joint Surgery, Department of Orthopedic Surgery, The Second Affiliated Hospital of Chongqing Medical University, 74 Linjiang Road, Chongqing, 400010, China. xianding@hospital.cqmu.edu.cn.
PMID: 38812038 DOI: 10.1186/s13018-024-04802-z
Abstract

Background: The larval zebrafish tail fin can completely regenerate in 3 days post amputation. mTOR, the main regulator of cell growth and metabolism, plays an essential role in regeneration. Lots of studies have documented the role of mTOR in regeneration. However, the mechanisms involved are still not fully elucidated.

Materials and results: This study aimed to explore the role and mechanism of mTOR in the regeneration of larval zebrafish tail fins. Initially, the spatial and temporal expression of mTOR signaling in the larval fin was examined, revealing its activation following tail fin amputation. Subsequently, a mTOR knockout (mTOR-KO) zebrafish line was created using CRISPR/Cas9 gene editing technology. The investigation demonstrated that mTOR depletion diminished the proliferative capacity of epithelial and mesenchymal cells during fin regeneration, with no discernible impact on cell Apoptosis. Insight from SMART-seq analysis uncovered alterations in the cell cycle, mitochondrial functions and metabolic pathways when mTOR signaling was suppressed during fin regeneration. Furthermore, mTOR was confirmed to enhance mitochondrial functions and CA2 + activation following fin amputation. These findings suggest a potential role for mTOR in promoting mitochondrial fission to facilitate tail fin regeneration.

Conclusion: In summary, our results demonstrated that mTOR played a key role in larval zebrafish tail fin regeneration, via promoting mitochondrial fission and proliferation of blastema cells.

Keywords

mTOR; Ca2+; Larvae fin; Mitochondrial fission; Regeneration; Zebrafish.

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