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Programmed cell death (PCD) is the deliberate suicide of an unwanted cell in a multicellular organism. In contrast to necrosis, which is a form of cell death that results from acute tissue injury and provokes an inflammatory response, PCD is carried out in a regulated process that generally confers advantages during an organism's life cycle. PCD serves fundamental functions during both plant and metazoa (multicellular animals) tissue development.

Types of programmed cell death

Programmed cell death has been classified into two main types:

  • Apoptosis (or Type I cell death), is a particular form of programmed cell death and is described in that article.
  • Autophagic (a.k.a. cytoplasmic, or Type II) cell death, characterized by the formation of large vacuoles that eat away organelles in a specific sequence before the nucleus is destroyed. [1]

Besides these two types of programmed cell death, other pathways have been discovered called "non-apoptotic programmed cell death" (or "caspase-independent programmed cell death" or "necrosis-like programmed cell death"). These alternative routes to death are as efficient as apoptosis and can function as backup mechanisms or as the main type of programmed cell death. For a review of these "new" pathways look at this paper in Nature Medicine "Caspase-Independent Cell Death" [5].

Plant cells undergo particular processes of programmed cell death, much more similar to autophagic cell death. However, some common features of PCD are highly conserved in both plants and metazoa.

The concept of "programmed cell death" was used in 1964 in relation to insect tissue development, around eight years before "apoptosis" was coined. Since then, PCD has become the more general of these terms. In other words, it refers to both apoptotic and nonapoptotic cell death pathways. Thus, it would not be correct to consider all forms of regulated cell death as "apoptosis".

The fact that programmed cell death has been the subject of increasing attention and research efforts was highlighted by the award of the 2002 Nobel Prize in Physiology or Medicine to Sydney Brenner (United Kingdom), H. Robert Horvitz (US) and John E. Sulston (UK) "for their discoveries concerning genetic regulation of organ development and programmed cell death" (see [6] ).

Evolutionary origin of PCD

Biologists had long suspected that mitochondria originated from bacteria that had been incorporated as endosymbionts (that is, a living body "living together inside") of larger, eukaryotic cells. It was Lynn Margulis who, since 1967, began championing this theory, which has since been widely accepted [2]. The most convincing evidence for this theory is the fact that mitochondria have their own DNA, and are equipped with their own genes and replication apparatus.

This evolutionary step would have been more than risky for the primitive eukaryotic cells that began to engulf energy-producing bacteria, and conversely, it must have been a perilous step for the ancestors of mitochondria that began to invade their proto-eukaryotic hosts. This process is still present today between human white blood cells and bacteria. Most of the time, invading bacteria are destroyed by the white blood cells; however, it is not uncommon for the chemical warfare waged by the prokaryotes to succeed, with the known consequences of infection, and the resulting damage.

One of those rare events in evolution, about two billion years before the present, must have made it possible for certain eukaryotes and energy-producing prokaryotes not only to coexist, but to mutually benefit from their symbiosis. [3]

Mitochondriate eukaryotic cells live poised between life and death, because mitochondria still retain their repertoire of molecules that can trigger cell suicide [4]. This process has now been evolved to happen only when programmed: given certain signals to cells, such as feedback from neighbors, stress or DNA damage, mitochondria release caspase activators that trigger the cell-death-inducing biochemical cascade. As such, the cell suicide mechanism is now crucial to life.

Programmed death of entire organisms

Main article: Phenoptosis

External Links


  1. Lawrence M. Schwartz et al.: "Do All Programmed Cell Deaths Occur Via Apoptosis?", PNAS 90(3) p. 980, 1 February. 1993[1]; and, for a more recent view, see W. Bursch et al.: "Programmed Cell Death (PCD): Apoptosis, Autophagic PCD, or Others?", Annals of the New York Academy of Sciences 926 p.1, 2000)[2].
  2. see "The Birth of Complex Cells", by Christian de Duve, Scientific American Vol. 274, 4, April, 1996
  3. See "Ancient Invasions: From Endosymbionts to Organelle", by Sabrina D. Dyall et al., Science Vol. 304 p. 253, 9 April. 2004[3].
  4. see Chiarugi and Moskowitz, in Science 297, p. 200[4]

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