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<p>Suspended animation, a state of profound metabolic, behavioral and developmental quiescence, is a remarkable yet poorly understood stress resilience strategy in animals. Here, we describe a previously uncharacterized form of suspended animation inducible by high-population density in isosmotic liquids in <i>C. elegans</i> throughout larval development and adulthood. Transcriptomic, metabolomic, and live-cell activity reporter imaging analyses reveal striking molecular and cellular landscape changes caused&#xa0;by such liquid-induced suspended animation (LISA), including remodeling of gene expression programs, energy metabolites, lysosomal and mitochondrial morphology. Genetic screens identify mutants with altered stress responses and survival against LISA. While key endo-lysosomal regulators promote survival during LISA, organelle remodeling and a neuronal axis via downstream neuropeptide and cAMP/PKA signaling orchestrate behavioral awakening from LISA. Our findings define a facile paradigm for reversible SA, providing a powerful model system to uncover key molecular and cellular mechanisms governing an extreme case of reversible life arrest and dormancy.</p>

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Induction and regulation of reversible suspended animation in C. elegans

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月31日

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  • Junqiang Liu,
  • Bingying Wang,
  • Jonathan Leon Catrow,
  • Quentinn Pearce,
  • Zhijian Ji,
  • Supeng Winnie Yang,
  • Akash Balakrishnan,
  • James E. Cox,
  • Dengke K. Ma

摘要

Suspended animation, a state of profound metabolic, behavioral and developmental quiescence, is a remarkable yet poorly understood stress resilience strategy in animals. Here, we describe a previously uncharacterized form of suspended animation inducible by high-population density in isosmotic liquids in C. elegans throughout larval development and adulthood. Transcriptomic, metabolomic, and live-cell activity reporter imaging analyses reveal striking molecular and cellular landscape changes caused by such liquid-induced suspended animation (LISA), including remodeling of gene expression programs, energy metabolites, lysosomal and mitochondrial morphology. Genetic screens identify mutants with altered stress responses and survival against LISA. While key endo-lysosomal regulators promote survival during LISA, organelle remodeling and a neuronal axis via downstream neuropeptide and cAMP/PKA signaling orchestrate behavioral awakening from LISA. Our findings define a facile paradigm for reversible SA, providing a powerful model system to uncover key molecular and cellular mechanisms governing an extreme case of reversible life arrest and dormancy.