Related Experiment Video
Updated: May 27, 2026
07:42
Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
Published on: June 29, 2011
Programmed cell death in plants: protective effect of mitochondrial-targeted quinones
L A Vasil'ev1, E V Dzyubinskaya, D B Kiselevsky
1Faculty of Biology, Lomonosov Moscow State University, Russia.
Biochemistry. Biokhimiia
|November 22, 2011
Summary
Synthetic quinone derivatives protect pea leaf cells from programmed cell death (PCD) at very low concentrations. These compounds, targeting mitochondria, offer novel insights into plant cell death pathways.
Area of Science:
- Plant Biology
- Cell Biology
- Biochemistry
Background:
- Programmed cell death (PCD) is a crucial process in plant development and stress response.
- Ubiquinone and plastoquinone are vital molecules in cellular energy metabolism.
- Understanding the mechanisms of PCD is essential for plant health and agriculture.
Purpose of the Study:
- To investigate the protective effects of synthetic quinone derivatives against PCD in pea leaf epidermis.
- To elucidate the role of mitochondria in plant PCD.
- To explore the impact of specific chemical inducers on different cell types.
Main Methods:
- Treatment of pea leaf epidermis with chitosan or cyanide (CN(-)) to induce PCD.
- Monitoring PCD by observing cell nuclei destruction.
- Utilizing synthetic ubiquinone and plastoquinone derivatives linked to cationic lipophilic groups (decyltriphenylphosphonium (DTPP(+)) and rhodamine).
- Assessing the influence of protonophoric uncouplers and tetraphenylphosphonium cations.
Main Results:
- Quinone derivatives, particularly DTPP(+) conjugates, prevented PCD induced by chitosan and CN(-) at pico- and nanomolar concentrations.
- CN(-) induced nuclear destruction in epidermal cells (EC) and guard cells (GC), while chitosan affected only EC.
- The protective effect was modulated by uncouplers and tetraphenylphosphonium, suggesting mitochondrial involvement.
- Certain derivatives suppressed menadione-induced H(2)O(2) generation and showed differential effects in light and dark conditions.
Conclusions:
- Cationic quinone derivatives are potent inhibitors of plant PCD, acting at very low concentrations.
- Mitochondria play a significant role in the execution of PCD in plant cells.
- The findings provide a basis for developing strategies to modulate plant cell death.
Related Concept Videos
01:22Cellular 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...
01:46Electron Transport Chain: Complex I and II
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
ROS generation is regulated and maintained at moderate levels necessary...
01:16Cellular Injury IV: Necrosis
Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
01:30The Electron Transport Chain
The electron transport chain or oxidative phosphorylation is an exothermic process in which free energy released during electron transfer reactions is coupled to ATP synthesis. This process is a significant source of energy in aerobic cells, and therefore inhibitors of the electron transport chain can be detrimental to the cell's metabolic processes.
Inhibitors of the electron transport chain
Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q in...
Inhibitors of the electron transport chain
Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q in...
01:31The Intrinsic Apoptotic Pathway
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
01:30Overview 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.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...