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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:
Besides these two types of programmed cell death other pathways are 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 main type of programmed cell death. For a review on these "new" pathways look at this Paper in Nature Medicine "Caspase-Independent Cell Death" {Link without Title} . 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". "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 January . 2001 {Link without Title} ). 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 {Link without Title} ). PROGRAMMED CELL DEATH IN PLANT TISSUE In "APL regulates vascular tissue identity in Arabidopsis", (by Martin Bonke ''et al.'', published in ''Nature'' Vol. 425, Nov. 13, 2003, p. 181.), 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 (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'', {Link without Title} ). 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 2004 , p. 305.) PROGRAMMED CELL DEATH IN SLIME MOULDS The social Slime Mould '' 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 subjected to food deprivation. The slug proceeds to grow a stalk, and, on top of it, a fruiting body that can disperse spores that will give birth to the next generation of ground-living, amoebae-like ''D. discoideum'' individuals {Link without Title} . 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. (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 {Link without Title} .) 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 mould, part of a branch that may have emerged from 2004 {Link without Title} .) EVOLUTIONARY ORIGIN OF PCD Biologists had long suspected that Mitochondria originated from Bacteria that had been incorporated as Endosymbiont s (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 Gene s 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 Cell s 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 . 2004 {Link without Title} .) Mitochondriate eukaryotic cells live poised between life and death, because mitochondria still retain their repertoire of molecules that can trigger cell suicide (see Chiarugi and Moskowitz, in '' Science '' 297, p. 200 {Link without Title} ). 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. SOURCES |
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