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Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
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Cellular Injury IlI: Cellular Death01:11

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A β-glucuronidase (GUS) Based Cell Death Assay
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Published on: May 6, 2011

Chitosan-induced programmed cell death in plants.

L A Vasil'ev1, E V Dzyubinskaya, R A Zinovkin

  • 1Biological Faculty, Lomonosov Moscow State University, Moscow, 119991, Russia.

Biochemistry. Biokhimiia
|November 18, 2009
PubMed
Summary

Chitosan induces programmed cell death in pea leaf epidermal cells (EC) through reactive oxygen species generated by NADPH oxidase. This process involves both apoptosis and autophagy, but does not affect stoma guard cells.

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Area of Science:

  • Plant biology
  • Cellular biology
  • Biochemistry

Background:

  • Chitosan is known to elicit defense responses in plants.
  • The precise mechanisms of chitosan-induced cell death are not fully understood.
  • Reactive oxygen species (ROS) play a role in plant cell death pathways.

Purpose of the Study:

  • To investigate the role of reactive oxygen species (ROS) in chitosan-induced epidermal cell (EC) death in pea leaves.
  • To elucidate the specific cellular pathways, including apoptosis and autophagy, involved in chitosan-induced EC death.
  • To identify the cellular sources of ROS production during chitosan treatment.

Main Methods:

  • Monitoring the destruction of cell nuclei in pea leaf epidermis.
  • Assessing hydrogen peroxide (H(2)O(2)) formation using 2',7'-dichlorofluorescein fluorescence.
  • Utilizing a range of inhibitors targeting specific cellular processes like NADPH oxidase, alternative oxidase, mitochondrial protein synthesis, cytoplasmic protein synthesis, and autophagy.
  • Analyzing DNA fragmentation patterns.

Main Results:

  • Chitosan induced EC death, characterized by nuclear condensation, DNA fragmentation, and internucleosomal DNA fragmentation, but spared stoma guard cells (GC).
  • Antioxidants and anaerobic conditions suppressed chitosan-induced EC death, indicating a role for ROS.
  • NADPH oxidase in the plasma membrane was identified as a primary source of ROS responsible for chitosan-induced EC death.
  • Chitosan-induced EC death involves a combination of apoptosis and autophagy, as evidenced by DNA fragmentation and the effect of autophagy inhibitors.

Conclusions:

  • Chitosan triggers programmed cell death in pea leaf epidermal cells via ROS generated by plasma membrane NADPH oxidase.
  • The cell death pathway initiated by chitosan involves both apoptotic and autophagic mechanisms.
  • Stoma guard cells are resistant to chitosan-induced cell death, suggesting specific cellular responses.