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Related Concept Videos

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.
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...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
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Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
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Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
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The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
The Intrinsic Apoptotic Pathway01:31

The 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...

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Updated: May 10, 2026

Studying Copper Nanoparticle-Induced Programmed Cell Death in Bacteria
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Studying Copper Nanoparticle-Induced Programmed Cell Death in Bacteria

Published on: May 16, 2025

mazEF-mediated programmed cell death in bacteria: "what is this?".

Bhaskar Chandra Mohan Ramisetty1, Bhargavi Natarajan, Ramachandran Sarojini Santhosh

  • 1School of Chemical and Biotechnology, SASTRA University , Thanjavur , India and.

Critical Reviews in Microbiology
|June 27, 2013
PubMed
Summary

Toxin-antitoxin systems, like mazEF in E. coli, trigger programmed cell death (PCD) under stress. This bacterial altruism may help populations survive by providing nutrients from dead cells.

Keywords:
Bacterial stress physiologyEscherichia coliextra cellular death factorpersistencetoxin–antitoxin systems

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LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

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Area of Science:

  • Microbiology
  • Molecular Biology
  • Bacterial Genetics

Background:

  • Toxin-antitoxin (TA) systems are prokaryotic genetic elements encoding toxins and antitoxins.
  • They are involved in bacterial persistence and programmed cell death (PCD).
  • The mazEF TA system is a well-studied Type II system in Escherichia coli.

Purpose of the Study:

  • To review the molecular mechanisms of mazEF TA system activation.
  • To examine the downstream consequences leading to bacterial cell death.
  • To evaluate the ecological advantages and disadvantages of the altruism hypothesis in bacterial populations.

Main Methods:

  • Review of existing literature on mazEF TA system.
  • Analysis of molecular pathways regulating mazEF-mediated PCD.
  • Ecological perspective on bacterial altruism and population survival.

Main Results:

  • Stress conditions like nutrient starvation and DNA damage activate mazEF-mediated PCD.
  • ppGpp and extracellular death factor are key regulators.
  • MazF toxin induces cell death via ribosome-independent RNA cleavage.
  • Programmed cell death may function as nutritional altruism, aiding population survival.

Conclusions:

  • The mazEF system plays a critical role in bacterial stress response and programmed cell death.
  • Nutritional altruism is a plausible ecological strategy for bacterial populations under duress.
  • Further research is needed to address experimental reproducibility and ecological validity.