PDF(Pubmed)
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.
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.
CONCLUSIONS: 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.
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.
CONCLUSIONS: 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.
摘要：
背景：幼体斑马鱼尾鳍可以在截肢后3天内完全再生。mTOR,细胞生长和代谢的主要调节剂，在再生中起着至关重要的作用。许多研究已经记录了mTOR在再生中的作用。然而,所涉及的机制仍未完全阐明。
结果：本研究旨在探讨mTOR在斑马鱼幼体尾鳍再生中的作用和机制。最初，检测了幼虫鳍中mTOR信号的时空表达，显示其激活后尾鳍截肢。随后，使用CRISPR/Cas9基因编辑技术创建了mTOR敲除（mTOR-KO）斑马鱼系。研究表明，mTOR耗竭减少了鳍再生过程中上皮细胞和间充质细胞的增殖能力，对细胞凋亡没有明显影响。来自SMART-seq分析的洞察力揭示了细胞周期的改变，鳍再生过程中mTOR信号受到抑制时线粒体功能和代谢途径。此外，mTOR被证实在截肢鳍后增强线粒体功能和Ca2+活化。这些发现表明mTOR在促进线粒体裂变以促进尾鳍再生中的潜在作用。
结论：总之，我们的研究结果表明，mTOR在斑马鱼尾鳍再生过程中发挥了关键作用，通过促进胚细胞的线粒体分裂和增殖。
结果：本研究旨在探讨mTOR在斑马鱼幼体尾鳍再生中的作用和机制。最初，检测了幼虫鳍中mTOR信号的时空表达，显示其激活后尾鳍截肢。随后，使用CRISPR/Cas9基因编辑技术创建了mTOR敲除（mTOR-KO）斑马鱼系。研究表明，mTOR耗竭减少了鳍再生过程中上皮细胞和间充质细胞的增殖能力，对细胞凋亡没有明显影响。来自SMART-seq分析的洞察力揭示了细胞周期的改变，鳍再生过程中mTOR信号受到抑制时线粒体功能和代谢途径。此外，mTOR被证实在截肢鳍后增强线粒体功能和Ca2+活化。这些发现表明mTOR在促进线粒体裂变以促进尾鳍再生中的潜在作用。
结论：总之，我们的研究结果表明，mTOR在斑马鱼尾鳍再生过程中发挥了关键作用，通过促进胚细胞的线粒体分裂和增殖。
