Programmed cell death 374215 220605727 2008-06-20T17:51:37Z DOI bot 6652755 Citation maintenance. You can [[WP:DOI|use this bot]] yourself! Please [[User:DOI_bot/bugs|report any bugs]]. Programmed cell-death ('''PCD''') is death of a [[cell (biology)|cell]] in any form, mediated by an intracellular program.<ref>{{cite journal|author=Engelberg-Kulka H, Amitai S, Kolodkin-Gal I, Hazan R|title=Bacterial Programmed Cell Death and Multicellular Behavior in Bacteria|year=2006|volume=2|issue=10|journal=PLoS Genetics|url=http://genetics.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pgen.0020135|pages=e135|doi=10.1371/journal.pgen.0020135}}</ref> In contrast to [[necrosis]], which is a form of cell-death that results from acute [[biological tissue|tissue]] injury and provokes an [[Inflammation|inflammatory]] response, PCD is carried out in a regulated [[process]] which generally confers advantage during an organism's [[life-cycle]]. PCD serves fundamental functions during both [[plant]] and [[metazoa]] (multicellular [[animal]]s) tissue development. *[[Apoptosis]] or Type I cell-death *[[autophagy|Autophagic]] or Type II cell-death ( ''[[cytoplasm]]ic'': characterized by the formation of large [[vacuoles]] which eat away [[organelles]] in a specific sequence prior to the [[cell nucleus|nucleus]] being destroyed.)<ref>{{cite journal|author=Lawrence M. Schwartz ''et al.''|title=Do All Programmed Cell Deaths Occur Via Apoptosis?|journal= PNAS|year=1993|volume= 90|issue=3 |pages= 980|doi= 10.1073/pnas.90.3.980|pmid=8430112}};and, for a more recent view, see {{cite journal|author=W. Bursch ''et al.''|title=Programmed Cell Death (PCD): Apoptosis, Autophagic PCD, or Others?|journal= Annals of the New York Academy of Sciences|year = 2000|volume=926|pages= 1|url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11193023}}</ref> Besides these two types of PCD, other pathways have been discovered.<ref>{{cite journal|author=Kroemer G, Martin SJ|title=Caspase-independent cell death|year=2005|volume=11|issue=7|pages=725–30|journal=Nat Med.|url=http://www.ncbi.nlm.nih.gov//entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16015365|doi=10.1038/nm1263}}</ref> 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 either backup mechanisms or the main type of PCD. Other forms of programmed cell death include [[anolkis]], almost identical to apoptosis except in its induction; [[cornification]], a form of cell death exlusive to the eyes; [[excitotoxicity]] and [[Wallerian degeneration]]. Plant cells undergo particular processes of PCD which are 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 by [[Richard_A._Lockshin|Lockshin]] & Williams<ref name="insect">{{cite journal | author=Richard A. Lockshin, Carroll M. Williams | title=Programmed cell death—II. Endocrine potentiation of the breakdown of the intersegmental muscles of silkmoths| journal=Journal of Insect Physiology| year=1964| volume=10| issue=4| pages=643–649| url=http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T3F-49N9JTD-BN&_user=10&_coverDate=08%2F31%2F1964&_alid=509668351&_rdoc=1&_fmt=summary&_orig=search&_cdi=4945&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=244d74b599c3c6e6979401175da87303 | doi=10.1016/0022-1910(64)90034-4}}</ref> 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 two terms. PCD has been the subject of increasing attention and research efforts. This trend has been highlighted with 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).<ref>2002 Nobel Prize in Medicine or Physiology[http://www.nobel.se/medicine/laureates/2002/index.html]</ref> == Programmed cell-death in plant tissue == In "APL regulates vascular tissue identity in [[Arabidopsis]]",<ref>Martin Bonke ''et al.'', published in ''Nature'' Vol. 425, Nov. 13, 2003, p. 181.</ref> [[Martin Bonke|Bonke]] and colleagues 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|cell-wall]] thickenings and programmed cell-death." The authors emphasize that the products of plant PCD play an important structural role. Basic morphological and biochemical features of PCD have been conserved in both plant and animal [[Kingdom (biology)|kingdoms]].<ref>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'', [http://www.plantcell.org/]</ref> 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 [[Cell nucleus|nuclear]] degradation being triggered by the collapse of the [[vacuole]] in [[Tracheid|tracheary]] elements of the xylem.<ref>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.</ref> [[Janneke Balk]] and [[Christopher J. Leaver]], of the Department of [[Department of Plant Sciences,University of Oxford|Plant Sciences]], [[University of Oxford]], carried out research on [[mutation]]s in the [[mitochondrial genome]] of [[Sunflower|sun-flower]] cells. Results of this research suggest that [[mitochondria]] play the same key role in vascular plant PCD as in other [[Eukaryote|eukaryotic]] cells.<ref>"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</ref> === PCD in pollen prevents inbreeding === During [[pollination]], plants enforce [[Self-incompatibility in plants|self-incompatibility]] ('''SI''') as an important means to prevent [[Biological reproduction|self-fertilization]]. Research on the [[corn poppy]] (''Papaver rhoeas'') has revealed that [[protein]]s in the [[pistil]] on which the [[pollen]] lands, interact with pollen and trigger PCD in incompatible (ie. ''self'') pollen. The researchers, [[Steven G. Thomas]] and [[Veronica E. Franklin-Tong]], also found that the response involves rapid inhibition of [[Pollen tube|pollen-tube]] growth, followed by PCD.<ref> Thomas, and Franklin-Tong: "Self-incompatibility triggers programmed cell death in Papaver pollen", ''Nature'' Vol. 429, 20 May 2004, p. 305.</ref> == Programmed cell death in slime molds == The social [[Slime mould|slime mold]] ''Dictyostelium [[Dictyostelid|discoideum]]'' has the peculiarity of adopting either a predatory [[amoeba]]-like behavior in its [[Microorganism|unicellular]] form, or coalescing into a mobile [[slug]]-like form when dispersing the [[spore]]s which will give birth to the next [[generation]].<ref>Crespi B, Springer S: "Ecology. Social slime molds meet their match" ''Science'' 2003 Jan 3;299(5603):105-6 [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12511635]. </ref> The stalk is composed of dead cells which have undergone a type of PCD that shares many features of an autophagic cell-death: massive vacuoles forming inside cells, a degree of [[chromatin]] condensation, but no [[Restriction digest|DNA-fragmentation]].<ref>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 [http://www.jcb.org/cgi/content/abstract/160/7/1105].</ref> The structural role of the residues left by the dead cells is reminiscent of the products of PCD in plant tissue. ''D. discoideum'' is a slime mold, part of a branch which may have emerged from [[Eukaryote|eukaryotic]] ancestors about a [[Timeline of evolution|billion years]] before the present. They apparently emerged after the ancestors of [[Viridiplantae|green-plants]] and the ancestors of [[fungi]] and animals had differentiated. But in addition to their place in the evolutionary [[Phylogenetic tree|tree]], the fact that PCD has been observed in the humble, simple, six-[[chromosome]] ''D. discoideum'' has additional significance: it permits the study of a developmental PCD path which does not depend on the caspases which are characteristic of apoptosis.<ref>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 [http://www.jbc.org/cgi/content/abstract/279/12/11489].</ref> == Evolutionary origin of PCD == Biologists had long suspected that [[mitochondria]] originated from [[bacterium|bacteria]] which had been incorporated as [[endosymbionts]] ("living together inside") of larger eukaryotic cells. It was [[Lynn Margulis]] who from [[1967]] on championed this [[theory]], which has since become widely accepted.<ref> see "The Birth of Complex Cells", by [[Christian de Duve]], ''[[Scientific American]]'' Vol. 274, 4, April, 1996</ref> The most convincing [[evidence]] for this theory is the fact that mitochondria possess their own [[DNA]] and are equipped with [[genes]] and [[DNA replication|replication]] apparatus. This [[evolution]]ary step would have been more than risky for the primitive eukaryotic cells which began to engulf the [[Electron transport chain|energy-producing]] bacteria and conversely, a perilous step for the ancestors of mitochondria which began to invade their proto-eukaryotic [[Host (biology)|hosts]]. This process is still evident today, between [[human]] white [[White blood cell| 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 [[chemical warfare|warfare]] waged by [[prokaryote]]s to succeed, with the consequence known as [[infection]] by its resulting damage. One of these rare evolutionary events, about [[Timeline of evolution|two billion years]] before the present, made it possible for certain eukaryotes and energy-producing prokaryotes not only to coexist, but to mutually benefit from their [[symbiosis]].<ref>See "Ancient Invasions: From Endosymbionts to Organelle", by Sabrina D. Dyall ''et al.'', ''Science'' Vol. 304 p. 253, 9 April. 2004[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15073369].</ref> Mitochondriate eukaryotic cells live poised between [[life]] and death, because mitochondria still retain their repertoire of [[molecule]]s which can trigger cell suicide.<ref>see Chiarugi and Moskowitz, in ''[[Science (journal)|Science]]'' 297, p. 200[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12114611]</ref> This process has now been evolved to happen only when programmed.{{Fact|date=April 2008}} Given certain [[Cell signaling|signals]] to cells (such as feedback from neighbors, stress or [[DNA repair|DNA-damage]]), mitochondria release [[caspase]] activators which trigger the cell-death inducing [[Biochemistry|biochemical]] cascade. As such, the cell-suicide [[Reaction mechanism|mechanism]] is now crucial to all of our lives. ==Programmed death of entire organisms== {{main|Phenoptosis}} ==External links== *[http://www.caspases.org Apoptosis and Cell Death Labs] *[http://www.celldeath-apoptosis.org International Cell Death Society] == Sources == {{reflist}} ==See also== {{embryology}} [[Category:Mitochondria]] [[Category:Programmed cell death|*]] [[ar:موت الخلية المبرمج]] [[de:Programmierter Zelltod]] [[et:Programmeeritud rakusurm]] [[he:מוות תאי מתוכנת]] [[hu:Programozott sejthalál]] [[ja:プログラム細胞死]] [[sl:Programirana celična smrt]] [[tr:Programlanmış hücre ölümü]] [[ur:برمجہ خلیاتی موت]] [[zh:细胞程序性死亡]]