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Programmed cell death
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==In plant tissue== Programmed cell death in plants has a number of molecular similarities to animal [[apoptosis]], but it also has differences, the most obvious being the presence of a [[cell wall]] and the lack of an [[immune system]] that removes the pieces of the dead cell. Instead of an immune response, the dying cell synthesizes substances to break itself down and places them in a [[vacuole]] that ruptures as the cell dies.<ref> {{cite journal |vauthors = Collazo C, Chacón O, Borrás O |year = 2006 |title = Programmed cell death in plants resembles apoptosis of animals |url = http://elfosscientiae.cigb.edu.cu/PDFs/BA/2006/23/1/BA002301RV001-010.pdf |journal = [[Biotecnología Aplicada]] |volume = 23 |pages = 1–10 |url-status = dead |archive-url = https://web.archive.org/web/20120314132513/http://elfosscientiae.cigb.edu.cu/PDFs/BA/2006/23/1/BA002301RV001-010.pdf |archive-date = 2012-03-14 }}</ref> In "APL regulates vascular tissue identity in [[Arabidopsis thaliana|Arabidopsis]]",<ref> {{cite journal |vauthors=Bonke M, Thitamadee S, Mähönen AP, Hauser MT, Helariutta Y |year = 2003 |title = APL regulates vascular tissue identity in Arabidopsis |journal = [[Nature (journal)|Nature]] |volume = 426 |issue = 6963 |pages = 181–6 |pmid = 14614507 |doi = 10.1038/nature02100 |bibcode = 2003Natur.426..181B |s2cid = 12672242 }}</ref> Martin Bonke and his colleagues had stated 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.{{cn|date=November 2024}} Basic morphological and biochemical features of PCD have been conserved in both plant and animal [[Kingdom (biology)|kingdoms]].<ref> {{cite journal |vauthors=Solomon M, Belenghi B, Delledonne M, Menachem E, Levine A |year = 1999 |title = The involvement of cysteine proteases and protease inhibitor genes in the regulation of programmed cell death in plants |journal = [[The Plant Cell]] |volume = 11 |issue = 3 |pages = 431–44 |pmid = 10072402 |pmc = 144188 |doi = 10.2307/3870871 |jstor=3870871 |bibcode = 1999PlanC..11..431S }} See also related articles in [http://www.plantcell.org/ ''The Plant Cell Online'']</ref> 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 triggered by the collapse of the [[vacuole]] in [[Tracheid|tracheary]] elements of the xylem.<ref> {{cite journal |vauthors=Ito J, Fukuda H |year = 2002 |title = ZEN1 Is a Key Enzyme in the Degradation of Nuclear DNA during Programmed Cell Death of Tracheary Elements |journal = [[The Plant Cell]] |volume = 14 | issue = 12 | pages = 3201–11 |pmid = 12468737 |pmc = 151212 |doi = 10.1105/tpc.006411 |bibcode = 2002PlanC..14.3201I }}</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 mutations 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> {{cite journal |vauthors=Balk J, Leaver CJ |year = 2001 |title = The PET1-CMS Mitochondrial Mutation in Sunflower Is Associated with Premature Programmed Cell Death and Cytochrome c Release |journal = [[The Plant Cell]] |volume = 13 | issue = 8 | pages = 1803–18 |pmid = 11487694 |pmc = 139137 |doi = 10.1105/tpc.010116 |bibcode = 2001PlanC..13.1803B }}</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 (i.e., ''self'') pollen. The researchers, Steven G. Thomas and [[Vernonica Franklin-Tong|Vernonica E. Franklin-Tong]], also found that the response involves rapid inhibition of [[Pollen tube|pollen-tube]] growth, followed by PCD.<ref> {{cite journal |vauthors=Thomas SG, Franklin-Tong VE |year = 2004 |title = Self-incompatibility triggers programmed cell death in Papaver pollen |journal = [[Nature (journal)|Nature]] |volume = 429 |issue = 6989 |pages = 305–9 |pmid = 15152254 |doi = 10.1038/nature02540 |bibcode = 2004Natur.429..305T |s2cid = 4376774 }}</ref>
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