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Related Concept Videos

Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

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Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
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Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
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Mitochondrial precursors are partially unfolded or loosely folded polypeptide chains. Newly synthesized precursors are inhibited from spontaneously folding into their native conformation by the cytosolic chaperones, heat shock proteins 70 (Hsp70), and mitochondrial import stimulation factors (MSFs). Precursors bound to MSFs are guided to the TOM70-TOM37 receptors, while precursors bound to Hsp70  chaperones are targetted to TOM20-TOM22 receptor complexes.
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Mitochondria01:37

Mitochondria

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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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Mitochondria are double-membrane organelles of the eukaryotes involved in cellular metabolism, signaling, ATP synthesis, and programmed cell death.  Each of these processes requires specific proteins and enzymes that must be correctly sorted to the right mitochondrial subcompartment for the proper functioning of the organelle.
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ATP Synthase: Mechanism01:48

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In animals, the mitochondrial F1F0 ATP synthase is the key protein that synthesizes ATP molecules through a complex catalytic mechanism. While the nuclear genome encodes the majority of ATP synthase subunits, the mitochondrial genome encodes some of the enzyme's most critical components. The formation of this multi-subunit enzyme is a complex multi-step process regulated at the level of transcription, translation, and assembly. Defects in one or more of these steps can result in decreased...
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Mitochondrial protein import is powered by two distinct energy sources: ATP hydrolysis and electrochemical potential across the inner membrane. Newly synthesized precursors are bound by cytosolic chaperones of the Hsp70 family, which guide them to the import receptors on the mitochondrial surface. Utilizing the energy of ATP hydrolysis, Hsp70 chaperones transfer these precursors to the TOM receptors on the mitochondrial outer membrane.
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Related Experiment Video

Updated: Mar 27, 2026

Assessment of Mitochondrial Fission/Fusion Dynamics in Kidney Proximal Tubular Cells
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Kif5 regulates mitochondrial movement, morphology, function and neuronal survival.

Diepiriye G Iworima1, Bryce A Pasqualotto1, Gordon L Rintoul1

  • 1Department of Biological Sciences, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.

Molecular and Cellular Neurosciences
|January 16, 2016
PubMed
Summary

Disrupting mitochondrial transport via kif5c in neurons altered mitochondrial shape, unexpectedly improving survival in some conditions. This suggests kif5c impacts neuronal health by regulating mitochondrial dynamics and function.

Keywords:
ATeamMitochondrial dynamicsMitochondrial remodelling, excitotoxicityMitochondrial traffickingkif5ro-GFP

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Mitochondrial Biology

Background:

  • Mitochondrial trafficking is crucial for neuronal health and function.
  • Compromised mitochondrial transport is implicated in neurodegenerative diseases.
  • KIF5C is a motor protein involved in intracellular transport.

Purpose of the Study:

  • To investigate the role of KIF5C-mediated mitochondrial trafficking in neuronal morphology and function.
  • To determine the impact of disrupted mitochondrial trafficking on neuronal survival under different toxic conditions.

Main Methods:

  • Primary rat cortical neurons were used.
  • Mitochondrial trafficking was disrupted using a dominant-negative KIF5C construct.
  • Mitochondrial morphology was assessed.
  • Reactive oxygen species (ROS) and ATP levels were measured using fluorescent probes.
  • Neuronal survival was evaluated following excitotoxicity and H2O2 exposure.

Main Results:

  • Disruption of KIF5C led to mitochondrial remodeling into punctate shapes, distinct from fission.
  • Neurons with punctate mitochondria showed decreased ROS and increased ATP levels.
  • Impaired mitochondrial trafficking enhanced neuronal survival during excitotoxicity.
  • Disruption of KIF5C exacerbated cell death induced by H2O2.

Conclusions:

  • KIF5C plays a novel role in regulating mitochondrial morphology beyond transport.
  • KIF5C-mediated mitochondrial dynamics are important for mitochondrial function and cellular health.
  • The effect of impaired mitochondrial trafficking on neuronal viability is context-dependent.