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Updated: Jun 15, 2025

Microfluidics-Assisted Selective Depolarization of Axonal Mitochondria
Published on: August 4, 2022
Axonal mitochondria regulate gentle touch response through control of axonal actin dynamics
Sneha Hegde1, Souvik Modi1, Ennis W Deihl2
1Tata Institute of Fundamental Research, Homi Bhabha Road, Navy Nagar, Colaba, Mumbai-400005, India.
Abstract:
Actin in neuronal processes is both stable and dynamic. The origin & functional roles of the different pools of actin is not well understood. We find that mutants that lack mitochondria, ric-7 and mtx-2; miro-1, in neuronal processes also lack dynamic actin. Mitochondria can regulate actin dynamics upto a distance ~80 μm along the neuronal process. Absence of axonal mitochondria and dynamic actin does not markedly alter the Spectrin Membrane Periodic Skeleton (MPS) in touch receptor neurons (TRNs). Restoring mitochondria inTRNs cell autonomously restores dynamic actin in a sod-2 dependent manner. We find that dynamic actin is necessary and sufficient for the localization of gap junction proteins in the TRNs and for the C. elegans gentle touch response. We identify an in vivo mechanism by which axonal mitochondria locally facilitate actin dynamics through reactive oxygen species that we show is necessary for electrical synapses & behaviour.
Insights
Mitochondria in neurons control actin dynamics, essential for electrical synapses and gentle touch behavior in C. elegans. This study reveals mitochondria
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Actin dynamics in neuronal processes are crucial for neuronal function but their origins and regulation remain unclear.
- Mitochondria are known to be vital for cellular energy but their specific roles in regulating neuronal actin dynamics are not well understood.
Purpose of the Study:
- To investigate the role of mitochondria in regulating actin dynamics within neuronal processes.
- To elucidate the mechanism by which mitochondria influence actin and its impact on neuronal function and behavior.
Main Methods:
- Utilized genetic mutants lacking mitochondria (ric-7, mtx-2; miro-1) in C. elegans touch receptor neurons (TRNs).
- Assessed actin dynamics, Spectrin Membrane Periodic Skeleton (MPS) integrity, and mitochondrial restoration.
- Examined the localization of gap junction proteins and C. elegans gentle touch response.
Main Results:
- Mutants lacking axonal mitochondria exhibited a loss of dynamic actin up to ~80 μm.
- Restoring mitochondria in TRNs rescued dynamic actin in a sod-2 dependent manner.
- Dynamic actin was found to be necessary and sufficient for gap junction protein localization and the gentle touch response.
Conclusions:
- Axonal mitochondria locally facilitate actin dynamics via reactive oxygen species, which is essential for electrical synapses and behavior.
- This study identifies a novel mechanism linking mitochondria, actin dynamics, and neuronal function in vivo.
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