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ROS and cGMP signaling modulate persistent escape from hypoxia in Caenorhabditis elegans.

Lina Zhao1,2,3, Lorenz A Fenk4, Lars Nilsson1,2,3

  • 1Umeå Centre for Molecular Medicine, Umeå University, Umeå, Sweden.

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Summary

Aerobic organisms need to detect oxygen shortages. This study reveals that reactive oxygen species (ROS) and cyclic GMP (cGMP) signaling regulate C. elegans

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Detecting and responding to acute oxygen (O2) shortages is vital for aerobic life.
  • The underlying molecular mechanisms and neural circuits for hypoxia response are not well understood.

Purpose of the Study:

  • To characterize the behavioral responses of *Caenorhabditis elegans* to acute hypoxia (approximately 1% O2).
  • To elucidate the molecular and circuit underpinnings of hypoxia avoidance and escape behaviors.

Main Methods:

  • Behavioral analysis of *C. elegans* feeding on 1% O2.
  • Genetic manipulation of phosphodiesterases (PDEs), G proteins, BBSome, mitochondrial complexes (MCI, MCIII), and GCY-28.
  • Optogenetic stimulation and Ca2+ imaging in neurons.

Main Results:

  • Acute hypoxia (1% O2) triggers turning and rapid forward movement in *C. elegans*.
  • Disruptions in PDEs, G proteins, BBSome, or increased reactive oxygen species (ROS) impair hypoxia escape.
  • Increased cyclic guanosine monophosphate (cGMP) signaling, primarily via GCY-28, inhibits hypoxia escape.
  • Mitochondrial dysfunction leading to high ROS abrogates acute hypoxia responses.

Conclusions:

  • Reactive oxygen species (ROS) and precise regulation of intracellular cyclic guanosine monophosphate (cGMP) are critical for modulating acute hypoxia responses in *C. elegans*.
  • Distinct molecular pathways, including cGMP signaling and mitochondrial function, govern responses to acute hypoxia.