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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" [9].

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 [10] ).

Programmed cell death in plant tissue

In "APL regulates vascular tissue identity in Arabidopsis", [2], Bonke and coworkers state that one of the two long-distance transport systems in vascular plants, xylem, consists of several cell types "the differentiation of which involves deposition of elaborate cell wall thickenings and programmed cell death." The authors emphasize that products of plant PCD play an important structural role.

Basic morphological and biochemical features of PCD have been conserved in both plant and animal kingdoms [3]. It should be noted, however, that specific types of plant cells carry out unique cell death programs. These have common features with animal apoptosis --for instance, nuclear DNA degradation--, but they also have their own peculiarities, such as nuclear degradation being triggered by the collapse of the vacuole in tracheary elements of the xylem. [4]

Janneke Balk and Christopher J. Leaver, of the Department of Plant Sciences, University of Oxford, carried out research on mutations in the mitochondrial genome of sun-flower cells. Results of this research suggest that mitochondria play the same key role in vascular plant programmed cell death as in other eukaryotic cells [5].

PCD in pollen prevents inbreeding

During polination, plants enforce self-incompatibility (SI) as an important means to prevent self-fertilization. Research on the corn poppy (Papaver rhoeas) has revealed that proteins in the pistil on which the pollen lands interact with pollen, and trigger programmed cell death in incompatible (self) pollen. The researchers, Steven G. Thomas and Veronica E. Franklin-Tong, also found that the response involves rapid inhibition of pollen-tube growth, followed by PCD. [6]

Programmed cell death in slime moulds

The social slime mold Dictyostelium discoideum has the peculiarity of adopting either a predatory amoeba-like behavior in its unicellular form, or coalescing into a mobile slug-like form when disperse spores that will give birth to the next generation of ground-living, amoebae-like D. discoideum individuals.[7]

The stalk is composed of dead cells that have undergone a type of PCD that shares many features of autophagic cell death: massive vacuoles forming inside these cells, a degree of chromatin condensation, but no DNA fragmentation. [8] The structural role of the residues left by dead cells is reminiscent of what has been discussed in relation to PCD in plant tissue.

D. discoideum is a slime mold, part of a branch that may have emerged from eukaryotic ancestors about a billion years before the present. They apparently emerged after the ancestors of green plants and the ancestors of fungi and animals had differentiated. But in addition to their place in the evolutionary tree, the fact that PCD has been observed in the humble, simple, six-chromosome D. discoideum has other significances as well: it permits the study of a developmental programmed cell death path that does not depend on the caspases that are characteristic of apoptosis. [9]

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 [10]. 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. [11]

Mitochondriate eukaryotic cells live poised between life and death, because mitochondria still retain their repertoire of molecules that can trigger cell suicide [12]. 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

Sources

  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. Martin Bonke et al., published in Nature Vol. 425, Nov. 13, 2003, p. 181.
  3. Mazal Solomon, et al.: "The Involvement of Cysteine Proteases and Protease Inhibitor Genes in the Regulation of Programmed Cell Death in Plants", The Plant Cell, Vol. 11, 431-444, March 1999. See also related articles in The Plant Cell Online, [3]
  4. See Jun Ito and Hiroo Fukuda: "ZEN1 Is a Key Enzyme in the Degradation of Nuclear DNA during Programmed Cell Death of Tracheary Elements", The Plant Cell, Vol. 14, 3201-3211, December 2002.
  5. "The PET1-CMS Mitochondrial Mutation in Sunflower Is Associated with Premature Programmed Cell Death and Cytochrome c Release", The Plant Cell, Vol. 13, 1803-1818, August 2001
  6. Thomas, and Franklin-Tong: "Self-incompatibility triggers programmed cell death in Papaver pollen", Nature Vol. 429, 20 May 2004, p. 305.
  7. [4].
  8. See the article by Levraud et al.: "Dictyostelium cell death : early emergence and demise of highly polarized paddle cells", The Journal of Cell Biology Vol. 160, 7, p. 1105 [5].
  9. See also Roisin-Bouffay et al.: "Developmental Cell Death in Dictyostelium Does Not Require Paracaspase", The Journal of Biological Chemistry Vol. 279, 12, p. 11489, 19 March 2004[6].
  10. see "The Birth of Complex Cells", by Christian de Duve, Scientific American Vol. 274, 4, April, 1996
  11. See "Ancient Invasions: From Endosymbionts to Organelle", by Sabrina D. Dyall et al., Science Vol. 304 p. 253, 9 April. 2004[7].
  12. see Chiarugi and Moskowitz, in Science 297, p. 200[8]

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