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Related Concept Videos

Actin Polymerization and Cell Motility01:13

Actin Polymerization and Cell Motility

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Actin is a family of globular proteins that are highly abundant in eukaryotic cells. It makes up approximately 1-5% of total cell protein concentration. Actin monomers polymerize to form a complex network of polarized filaments, the actin cytoskeleton, that plays a crucial role in many cellular processes, including cell motility, division, endocytosis, and metastasis of cancer cells.
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Actin Treadmilling01:18

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Actin filaments undergo polymerization and depolymerization from either end. The polymerization and depolymerization rates depend on the cytosolic concentration of free G-actins. The polymerization rate is generally higher at the plus or barbed end, while the depolymerization rate is higher at the minus or pointed end. At a steady state, critical concentration describes the concentration of free G-actin monomers at which the polymerization rate at the plus end is equal to that of the...
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Actin Polymerization01:42

Actin Polymerization

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Actin polymerization occurs through the head-to-tail association of binding sites on monomeric actin or G-actin to form filamentous or F-actin. The polymerization can be divided into three phases ̶  nucleation, elongation, and steady-state phase.
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Actin filaments (F-actin) are composed of actin subunits. The dissociation of actin monomers can occur from either end of F-actin. The rate of dissociation is faster from the minus-end or the pointed end, where the actin subunits exist with a bound ADP, together known as ADP-actin. The depolymerization of F-actin is aided by proteins, including the actin-depolymerizing factor (ADF) and cofilin family of proteins, gelsolin, and glia maturation factor (GMF).
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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 Membranes01:45

Mitochondrial Membranes

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A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
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Mitochondrial dysfunction triggers actin polymerization necessary for rapid glycolytic activation.

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Acute damage-induced actin (ADA) polymerization around mitochondria rapidly activates glycolysis. This cellular response helps re-establish ATP production following mitochondrial damage, crucial for cell survival.

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Area of Science:

  • Cell Biology
  • Mitochondrial Biology
  • Metabolism

Background:

  • Mitochondrial damage disrupts cellular homeostasis.
  • Perimitochondrial actin polymerization, termed acute damage-induced actin (ADA), is a rapid cellular response to mitochondrial damage.
  • The functional consequences of ADA remain largely unknown.

Purpose of the Study:

  • To investigate the role of ADA in cellular responses to mitochondrial damage.
  • To determine the link between ADA and cellular energy metabolism.
  • To explore ADA's involvement in ATP production restoration.

Main Methods:

  • Utilized mouse embryonic fibroblasts and CD8+ T lymphocytes.
  • Induced mitochondrial damage using various chemical agents (CCCP, antimycin, rotenone, oligomycin) and hypoxia.
  • Inhibited ADA and glycolytic activation using Arp2/3 complex inhibitor (CK666) and NCLX inhibitor (CGP37157).
  • Examined chronic mitochondrial dysfunction models (mtDNA depletion, NDUFS4 mutation).

Main Results:

  • ADA was observed in response to diverse mitochondrial damage inducers.
  • Inhibition of ADA also suppressed rapid glycolytic activation.
  • Chronic mitochondrial dysfunction led to persistent perimitochondrial actin filaments.
  • Arp2/3 inhibition in NDUFS4 knock-out cells caused actin loss and reduced ATP.

Conclusions:

  • ADA is a key mediator of rapid glycolytic activation following mitochondrial damage.
  • ADA plays a crucial role in maintaining cellular ATP levels under conditions of mitochondrial impairment.
  • This mechanism is conserved across different cell types and contributes to cellular resilience.