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Related Concept Videos

Delivery Pathways to the Lysosome01:36

Delivery Pathways to the Lysosome

Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
Endocytosis
In endocytosis, the cell membrane takes up macromolecules and particles from the surrounding medium. Clathrin-mediated...
Autophagy01:27

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
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Autophagic Cell Death01:18

Autophagic Cell Death

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Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
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IP3/DAG Signaling Pathway01:11

IP3/DAG Signaling Pathway

Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the  phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and produces two-second...

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Related Experiment Video

Updated: Jun 5, 2026

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy
07:20

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy

Published on: January 31, 2025

The phospholipase D1 pathway modulates macroautophagy.

Claudia Dall'Armi1, Andrés Hurtado-Lorenzo, Huasong Tian

  • 1Department of Pathology and Cell Biology, Columbia University Medical Center, New York, New York 10032, USA.

Nature Communications
|January 27, 2011
PubMed
Summary
This summary is machine-generated.

Phospholipase D1 (PLD1) regulates autophagy, a cellular degradation process. This study shows PLD1 is crucial for autophagosome expansion and clearing protein aggregates like Tau.

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Macroautophagy is a vital cellular process for degrading cytoplasmic components via autophagosomes fusing with lysosomes.
  • The specific lipid modifications governing autophagosomal membrane dynamics remain largely unknown.

Purpose of the Study:

  • To investigate the role of phospholipase D1 (PLD1) in the lipid dynamics and regulation of macroautophagy.

Main Methods:

  • Tracking PLD1 localization in response to nutrient starvation.
  • Assessing PLD activity and its modulation by wortmannin (a PI3K inhibitor).
  • Evaluating the impact of PLD inhibition and PLD1 genetic ablation on autophagy markers (LC3-positive compartments) and protein aggregate levels (Tau, p62) in cellular and brain slice models.

Main Results:

  • Nutrient starvation induces partial relocalization of PLD1 to autophagosome-like structures.
  • PLD1 localization and starvation-induced PLD activity are influenced by wortmannin, suggesting PLD1 acts downstream of Vps34.
  • Inhibition of PLD or genetic deletion of PLD1 impairs starvation-induced autophagosome expansion.
  • PLD inhibition increases Tau and p62 aggregate levels in brain slices.

Conclusions:

  • Phospholipase D1 (PLD1) plays a significant role in regulating autophagy.
  • PLD1 is involved in the expansion of autophagosome-related compartments.
  • PLD1 activity is linked to the clearance of protein aggregates, suggesting its therapeutic potential in neurodegenerative diseases.