Programmed cell death

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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.

Table of contents

1 Types of programmed cell death
2 Programmed cell death in plant tissue

2.1 PCD in pollen prevents inbreeding

3 Evolutionary origin of PCD

Types of programmed cell death

Programming 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. (See Lawrence M. Schwartz et al.: "Do All Programmed Cell Deaths Occur Via Apoptosis?", PNAS 90(3) p. 980, 1 Feb. 1993; and, for a more recent view, see W. Bursh et al.: "Programmed Cell Death (PCD): Apoptosis, Autophagic PCD, or Others?", Annals of the New York Academy of Sciences 926 p.1, 2000).

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 autophagic and apoptotic cell death pathways. Thus, it would not be correct to consider all forms of regulated cell death as "apoptosis".

"Physiological cell death" has also been used as a general term to cover different sequences and morphologies (see Richard Lockshin and Zahra Zakeri: "Programmed cell death and apoptosis: origins of the theory", Nature Reviews Molecular Cell Biology 2 p. 545, 1 Jan. 2001).

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 (Great Britain), H. Robert Horvitz (US) and John E. Sulston (GB) "for their discoveries concerning genetic regulation of organ development and programmed cell death" (see [1] ).

Programmed cell death in plant tissue

Although research on programmed cell death (PCD) in plants has not received the sort of attention enjoyed in top scientific journals by its animal counterpart, the role played by PCD in development and sculpturing of vascular plant tissue has not altogether been lost or played down by our "animal kingdom comes first" prejudice. All wikipedians interested in cell biology should be delighted to find "APL regulates vascular tissue identity in Arabidopsis", by Martin Bonke et al., published in Nature Vol. 425, Nov. 13, 2003, p. 181. Even though their article is not specifically focused on PCD, Bonke and coworkers tell us 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 (see 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, [1]). 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. (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.)

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 (see "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).

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 polen lands interact with pollen, and triggers programmed cell death in incompatible (self) pollen. The researchers, Steven G. Thomas and Veronica E. Franklin-Tong, also found out that the response involves rapid inhibition of pollen-tube growth, followed by PCD. (See Thomas, and Franklin-Tong: "Self-incompatibility triggers programmed cell death in Papaver pollen", Nature Vol. 429, 20 May 2004, p. 305.)

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, that has since been widely accepted (see "The Birth of Complex Cells", by Christian de Duve, Scientific American Vol. 274, 4, April, 1996). 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 must have been more than risky for the primitive eukaryotic cells that began to engulf energy-producing bacteria --or, conversely, it must have been a perilous step for the ancestors of mitochondria that began to invade their proto-eukaryotic hosts. The drama is still enacted today in our own white blood cells (which, it must be said, are much better equipped to entrap and destroy bacteria that intend to invade our bodies). Most of the time, invading bacteria are destroyed by the white blood cells; but, oftentimes, the chemical warfare waged by the prokaryotes succeeds, 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. (See "Ancient Invasions: From Endosymbionts to Organelle", by Sabrina D. Dyall et al., Science Vol. 304 p. 253, 9 Apr. 2004.)

In a very real and immediate sense, it can be said that eukaryotic cells live poised between life and death, because mitochondria still retain their repertoire of molecules that can trigger cell suicide (see the afore-quoted article by Chiarugi and Moskowitz, in Science 297, p. 200). Given certain signals or insults to cells—such as feed-back from neighbors, stress or DNA damage—mitochondria release caspase activators that produce the cell-death-inducing biochemical cascade.

As previously explained in this article, however, this fine equilibrium between life and death that all of us eukaryotic beings carry most intimately and deeply, is essential to life.