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Related Concept Videos

Electron Transport Chain: Complex I and II01:46

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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
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The mitochondrial cristae membrane is the primary site for the oxidative phosphorylation (OXPHOS) process of energy conversion mediated through respiratory complexes I to V. These complexes have been widely studied for decades, and it has been proven that they form supramolecular structures called respiratory supercomplexes (SC). These higher-order complexes may be crucial in maintaining the biochemical structure and improving the physiological activity of the individual complexes while...
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Updated: Sep 24, 2025

An Anoxia-starvation Model for Ischemia/Reperfusion in C. elegans
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A reversible mitochondrial complex I thiol switch mediates hypoxic avoidance behavior in C. elegans.

John O Onukwufor1,2, M Arsalan Farooqi1, Anežka Vodičková1

  • 1Department of Anesthesiology and Perioperative Medicine, University of Rochester Medical Center, Rochester, NY, 14642, USA.

Nature Communications
|May 3, 2022
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Summary
This summary is machine-generated.

Worm behavior changes due to metabolic distress are controlled by specific mitochondrial reactive oxygen species (ROS) production. This site-specific ROS, linked to Complex I, is crucial for adapting to low oxygen (hypoxia).

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Area of Science:

  • Cellular Biology
  • Neuroscience
  • Biochemistry

Background:

  • Metabolic distress in C. elegans triggers behavioral changes coordinated by redox-sensitive mitochondrial processes.
  • Mitochondrial Complex I is a key site for reactive oxygen species (ROS) production, linked to oxidative damage during hypoxia.

Purpose of the Study:

  • To investigate the role of spatiotemporal ROS production in coordinating behavioral responses to metabolic distress.
  • To elucidate the molecular mechanisms underlying redox-sensitive regulation of behavior during hypoxia.

Main Methods:

  • Utilized optogenetics and CRISPR/Cas9 genome editing for spatiotemporal control of ROS production.
  • Employed molecular modeling to understand the impact of thiol oxidation on Complex I function.

Main Results:

  • Demonstrated that localized ROS production, via reversible thiol oxidation on NDUF-2.1, drives photo-locomotory remodeling and avoidance behavior.
  • Showcased that this specific thiol oxidation is necessary and sufficient for hypoxic behavioral responses and protects against lethal hypoxia.
  • Revealed that oxidation destabilizes the Q-binding pocket in NDUF-2.1, decreasing Complex I activity.

Conclusions:

  • Site-specific ROS production by mitochondrial Complex I is a critical regulator of behavioral adaptation to hypoxia.
  • Reversible oxidation of a specific thiol on NDUF-2.1 mediates behavioral responses and confers protection against hypoxia.
  • Targeting this site-specific ROS production offers a potential strategy to mitigate hypoxia's detrimental effects.