Tesis sobre el tema "Programmed cell death"
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Courtois-Moreau, Charleen Laetitia. "Programmed Cell Death in Xylem Development". Doctoral thesis, Umeå universitet, Umeå Plant Science Centre, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1831.
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Concerns about climate changes and scarcity of fossil fuels are rising. Hence wood is becoming an attractive source of renewable energy and raw material and these new dimensions have prompted increasing interest in wood formation in trees, in both the scientific community and wider public. In this thesis, the focus is on a key process in wood development: programmed cell death (PCD) in the development of xylem elements. Since secondary cell wall formation is dependent, inter alia, upon the life time of xylem elements, the qualitative features of wood will be affected by PCD in xylem, about which there is little information. This thesis focuses on the anatomical, morphological and transcriptional features of PCD during xylem development in both the stem of hybrid aspen, Populus tremula (L.) x tremuloides (Michx.) and the hypocotyl of the herbaceous model system Arabidopsis thaliana (L. Heynh.). In Populus, the progressive removal of organelles from the cytoplasm before the time of death (vacuolar bursts) and the slowness of the cell death process, illustrated by DNA fragmentation assays (such as TUNEL and Comet assays), have been ascertained in the xylem fibres by microscopic analyses. Furthermore, candidate genes for the regulation of fibre cell death were identified either from a Populus EST library obtained from woody tissues undergoing fibre cell death or from microarray experiments in Populus stem, and further assessed in an in silico comparative transcriptomic analysis of Arabidopsis thaliana. These candidate genes were either putative novel regulators of fibre cell death or members of previously described families of cell death-related genes, such as autophagy-related genes. The induction of the latter and the previous microscopic observations suggest the importance of autophagy in the degradation of the cytoplasmic contents specifically in the xylem fibres. Vacuolar bursts in the vessels were the only previously described triggers of PCD in the xylem, which induce the very rapid degradation of the nuclei and surrounding cytoplasmic contents, therefore unravelling a unique previously unrecorded type of PCD in the xylem fibres, principally involving autophagy. Arabidopsis is an attractive alternative model plant for exploring some aspects of wood formation, such as the characterisation of negative regulators of PCD. Therefore, the anatomy of Arabidopsis hypocotyls was also investigated and the ACAULIS5 (ACL5) gene, encoding an enzyme involved in polyamine biosynthesis, was identified as a key regulator of xylem specification, specifically in the vessel elements, though its negative effect on the cell death process. Taken together, PCD in xylem development seems to be a highly specific process, involving unique cell death morphology and molecular machinery. In addition, the technical challenges posed by the complexity of the woody tissues examined highlighted the need for specific methods for assessing PCD and related phenomena in wood.Oron för klimatförändringar och brist på fossila bränslen har ökat påtagligt under de senaste åren. De enorma möjligheter som skogsråvaran erbjuder som alternativ källa för förnyelsebar energi och råmaterial har väckt ett stort intresse också för den biologiska processen bakom vedbildning i träd. Denna avhandling fokuserar på en viktig process i vedbildning: programmerad celldöd (PCD) i xylemet. Xylemcellernas livstid påverkar bildningen av sekundära cellväggar, vilket i sin tur påverkar vedens kvalitativa egenskaperna, så som veddensitet. Trots dess betydelse för viktiga egenskaper hos vedråvaran existerar fortfarande väldigt lite information om xylem PCD på cellulär eller molekylär nivå. I den här avhandlingen belyses de anatomiska, morfologiska och genetiska aspekterna av PCD i xylemutveckling i både stam av hybridasp, Populus tremula (L.) x tremuloides (Michx.) och hypokotyl av det örtartade modellsystemet Arabidopsis thaliana (L. Heynh.). Xylemet i både Populus och Arabidopsis består av två olika celltyper; de vattentransporterade kärlen och de stödjande fibrerna. Det är känt att celldöd i kärlen pågår mycket snabbt efter att den centrala vakuolen brister och de hydrolytiska enzymer släpps in i cytoplasman. I den här avhandlingen ligger fokus på fibrerna i Populus xylemet. Med hjälp av mikroskopianalyser av cellmorfologin (elektronmikroskopi) och DNA-fragmentering i cellkärnan (TUNEL- och Comet-analyser) kunde vi konstatera att till skillnad från kärlen så uppvisar fibrerna en långsam och progressiv nedbrytning av organellerna och cellkärnans DNA före vakuolbristning. Dessutom har kandidatgener för reglering av fibercelldöd identifierats antingen från ett Populus EST bibliotek från vedartade vävnader som genomgår fibercelldöd eller från mikroarray experiment i Populus stam. Dessa kandidatgener är antingen potentiella nya regulatorer av fibercelldöd eller medlemmar av tidigare beskrivna familjer av celldödsrelaterade gener. Bland de sistnämnda finns autofagi-relaterade gener, vilket stöder funktionen av autofagi i samband med autolys av cellinnehållet i xylemfibrerna. Dessa studier pekar därför på en typ av PCD som har inte tidigare beskrivits för xylemet. Arabidopsis är ett alternativt växtmodellsystem för studier av vissa aspekter av vedbildningen, såsom karakteriseringen av negativa regulatorer av PCD. Därför har också hypokotylanatomin analyserats, och ACAULIS5 (ACL5) genen, som kodar för ett enzym i biosyntesen av polyaminer, har visats vara en viktig regulator av xylemspecifikation genom dess negativa effekt på kärlens celldöd. Sammantaget visar denna avhandling att PCD i xylemutvecklingen verkar involvera unika morfologiska och molekylära mekanismer. Vi visar dessutom att komplexiteten hos de vedartade vävnaderna leder till ett behov av bättre anpassade verktyg för att djupare kunna bedöma PCD och liknande fenomen i veden.
Även med namnet Moreau-Courtois, Charleen L. samt Moreau, Charleen.
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Świdziński, Jodi A. "Programmed cell death in Arabidopsis thaliana". Thesis, University of Oxford, 2003. http://ora.ox.ac.uk/objects/uuid:6e2580fc-8873-4722-89f7-b206d4be2a5f.
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Programmed Cell Death (PCD) describes an orderly cellular breakdown that occurs in both plants and animals throughout development and in response to biotic and abiotic stresses. The molecular machinery that functions in the induction and execution of animal PCD has been characterised in great detail. Conversely, few genes and proteins involved in plant PCD have been identified. While certain features of animal PCD may be conserved, the induction and execution of plant PCD is also likely to involve novel proteins and mechanisms. The aim of the work presented in this thesis was to investigate experimental approaches for studying plant PCD and to gain an understanding of the molecular mechanisms involved. To this end, an Arabidopsis thaliana cell suspension system was developed in which PCD could be induced by both a heat treatment (55°C, 10 min) and senescence (13 to 14 days-old). This system allowed for the molecular responses related to programmed cell death to be distinguished from those that were a specific response to the inducing stimulus. The Arabidopsis cell suspension system was utilised for an analysis of transcriptomic and proteomic changes that occur following the induction of PCD. A custom cDNA microarray analysis of ~100 putative cell death-related genes was used to measure the abundance of transcripts of these genes during PCD, and this work was extended to a whole-genome transcriptomic analysis of PCD. A number of candidate genes that may play a role in plant PCD were identified. These included those encoding antioxidant enzymes, cytosolic heat shock proteins, the mitochondrial adenine nucleotide translocase, ion transporters, a two-component response regulator (ARR4), several pathogenesis-related proteins, phospholipases and proteases, extracellular glycoproteins and enzymes (including a subtilisin-like protease, chitinases, and glucanases), and transcriptional regulators such as a homeobox leucine zipper and NAC-domain proteins. The induction and execution of plant PCD is also likely to involve mechanisms that are not transcriptionally regulated. A proteomic analysis of changes in the total cellular protein profile during heat- and senescence-induced PCD was therefore used to identify 12 proteins that are modulated in both systems and may play a PCD-specific role. These included the mitochondrial voltage-dependent anion channel (Athsr2), catalase, mitochondrial superoxide dismutase, an extracellular glycoprotein, and aconitase. Selected genes and proteins identified in the transcriptomic and proteomic analyses were further investigated in an attempt to define their role in plant PCD. Since PCD is difficult to quantitatively analyse at the whole-plant level, initially a strategy of transient expression of genes of interest in Arabidopsis protoplasts was adopted. However, it proved to be technically difficult to accurately quantify the number of dead cells in this system. As an alternative, Arabidopsis T-DNA insertional mutants within genes of interest were investigated for PCD-related phenotypes. Mutants in Senescence-Related Gene 3, the mitochondrial voltage-dependent anion channel (Athsr2), and cytosolic Heat shock protein 70-3 were isolated. The mutant lines were not visibly affected in their development, formation of xylem, onset and progression of senescence, or responses to abiotic and biotic stresses. This indicated that these genes are either not involved in the PCD pathway or that their functional role can be fulfilled by other gene products.
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Sharma, Pundrique Radheyshyam. "Programmed cell death during heart development". Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272255.
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Palazzo, Francesco Fausto. "Programmed cell death in autoimmune thyroid disease". Thesis, Queen Mary, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270709.
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Wilkinson, Derek. "Proteases and programmed cell death in fungi". Thesis, University of Exeter, 2011. http://hdl.handle.net/10036/3629.
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Programmed cell death in animals, plants and protists is in part regulated by a variety of proteases, including cysteine aspartyl proteases, (caspases, paracaspases and metacaspases), cathepsins, subtilisin-like serine proteases, vacuolar processing enzymes and the proteasome. The role of different proteases in the cell death responses of the fungi is however largely unknown. A greater understanding of the fungal cell death machinery may provide new insights into the mechanisms and evolution of PCD and potentially reveal novel targets for a new generation of antifungal drugs. The role of a metacaspase encoding gene, MCA1, in the cell death response of the human pathogen Candida albicans pathogen has been investigated by functional analysis. MCA1 deletion not only alters the sensitivity of cells to a number of cell death stimuli, it also enhances virulence in an insect model. C. albicans shows altered cell and colony morphology on Lee’s medium. Evidence is presented to suggest that these functions appear to be dependent upon active mitochondria. In this study it has also been shown that key caspase substrates may be conserved between humans and the yeasts Saccharomyces cerevisiae and Candida albicans. Many substrates, particularly those which are essential, have retained their caspase cleavage motifs. 14 protease mutants displayed altered activity against caspase 1, 3, 6 or 8 substrates during acetic acid-induced PCD and caspase 1-like activity appeared to be particularly associated with PCD. Using a novel bioinformatic analysis of experimental LC-MS/MS data, changes in the degradation patterns of the proteome (destructome) following acetic acid-induced cell death have been investigated in wild-type yeast. In addition, potential native substrates of the yeast Mca1 have also been identified. The future challenge is to characterise the destructome of different proteases under a range of cell death conditions. In this way it may be possible to identify key components of the cell death machinery and their substrates and so reveal the most promising targets for future therapeutics.
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Jagasia, Ravi. "Mitochondrial dynamics in Caenorhabditis elegans programmed cell death". Diss., [S.l.] : [s.n.], 2005. http://edoc.ub.uni-muenchen.de/archive/00004281.
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Cowling, Victoria Haigh. "Regulation of capase activation during programmed cell death". Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397249.
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Drury, Georgina E. "UVC-induced programmed cell death in Arabidopsis thaliana". Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.678199.
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Cameron, Angus Crawford. "The control of physiological programmed cell death : apoptosis". Thesis, The University of Sydney, 1991. http://hdl.handle.net/2123/4751.
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Nelson, Charles J. "MicroRNA Regulation of Autophagy during Programmed Cell Death: A Dissertation". eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/756.
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Autophagy delivers cytoplasmic material to the lysosome for degradation, and has been implicated in many cellular processes, including stress, infection, survival, and death. Although the regulation and role that autophagy plays in stress, infection, and survival is apparent, its involvement during cell death remains relatively unclear. In this thesis I summarize what is known about the roles autophagy can play in cell death, and the differences between the utilization of autophagy during nutrient deprivation and cell death. Utilizing Drosophila melanogaster as a model system, the roles autophagy plays in both of these contexts can be studied. The goal of this thesis is to provide a better understanding of the regulatory mechanisms that distinguish between autophagy as a survival mechanism and autophagy as a cell death mechanism. From my studies I was able to determine that microRNAs can regulate autophagy in vivo, and that the microRNA miR-14 controls autophagy specifically during the destruction of the larval salivary glands of Drosophila melanogaster. I found that miR-14 regulates autophagy through modulation of IP3 and calcium signaling, and this miR-14 control of IP3 and calcium signaling does not influence the induction of autophagy during nutrient deprivation. Therefore, this knowledge demonstrates how autophagy can be regulated to distinguish its use during cell survival and death providing insight into how autophagy can used to treat diseases.
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Nelson, Charles J. "MicroRNA Regulation of Autophagy during Programmed Cell Death: A Dissertation". eScholarship@UMMS, 2003. http://escholarship.umassmed.edu/gsbs_diss/756.
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Autophagy delivers cytoplasmic material to the lysosome for degradation, and has been implicated in many cellular processes, including stress, infection, survival, and death. Although the regulation and role that autophagy plays in stress, infection, and survival is apparent, its involvement during cell death remains relatively unclear. In this thesis I summarize what is known about the roles autophagy can play in cell death, and the differences between the utilization of autophagy during nutrient deprivation and cell death. Utilizing Drosophila melanogaster as a model system, the roles autophagy plays in both of these contexts can be studied. The goal of this thesis is to provide a better understanding of the regulatory mechanisms that distinguish between autophagy as a survival mechanism and autophagy as a cell death mechanism. From my studies I was able to determine that microRNAs can regulate autophagy in vivo, and that the microRNA miR-14 controls autophagy specifically during the destruction of the larval salivary glands of Drosophila melanogaster. I found that miR-14 regulates autophagy through modulation of IP3 and calcium signaling, and this miR-14 control of IP3 and calcium signaling does not influence the induction of autophagy during nutrient deprivation. Therefore, this knowledge demonstrates how autophagy can be regulated to distinguish its use during cell survival and death providing insight into how autophagy can used to treat diseases.
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Asavaritikrai, Pundit. "Regulation of programmed cell death in the developing thalamus". Thesis, University of Edinburgh, 2000. http://hdl.handle.net/1842/24709.
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In this thesis, I examined PCD in the thalamus during the period of innervation of the cortex (late embryonic to early postnatal ages in mice). I found that apoptosis (revealed by TUNEL and pyknotic morphology) is a common mode of thalamic PCD both in vivo and in vitro. In vivo studies showed the highest rate of cell death is in early postnatal life, at postnatal day 1 (P1). In vivo analysis of animals lacking functional neurotrophin tyrosine kinase receptors, TrkB and TrkC, and in vitro work in collaboration with Dr Beau Lotto showed that brain-derived neurotrophic factor (BDNF), acting via TrkB, regulates thalamic survival in the perinatal period. My in vitro studies showed that thalamic cells cultured from E15 for up to 5 days showed a loss of viability after 2-3 days, which precedes the in vivo increase in thalamic PCD. Cortical factors in addition to BDNF are able to maintain thalamic viability for longer periods in culture. Later studies showed that these factors are not unique to the cerebral cortex but can be found in other neuronal tissues. Amongst other tissues, the late-gestation thalamus is able to produce them provided it is stimulated with elevated levels of K+. Elevated K+ is known to promote thalamic survival by increasing depolarisation but I found evidence that elevated K+ did not require TrkB or TrkC signaling to produce a trophic effect since K+ had normal trophic effects on the thalamic explants of either trkB (-/-) or trkC (-/-) animals. Moreover, I observed an increased cell death in the E19 thalamus in mice homozygous for a mutation of the transcription factor pax-6. This mutant is known to lack thalamocortical innervation and my in vivo and in vitro analysis of this mutant, suggested that thalamocortical innervation is essential for developing thalamic cells to obtain sufficient trophic factors.
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Helmersson, Andreas. "Programmed cell death and genetic stability in conifer embryogenesis /". Uppsala : Dept. of Plant Biology and Forest Genetics, Swedish University of Agricultural Sciences, 2007. http://epsilon.slu.se/2007127.pdf.
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Thomas, Marshall Peter. "Novel Roles for Ribonucleic Acids in Programmed Cell Death". Thesis, Harvard University, 2014. http://nrs.harvard.edu/urn-3:HUL.InstRepos:13094353.
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Apoptosis is a tightly coordinated program to shut down and dismantle a cell, characterized by mitochondrial outer membrane permeabilization (MOMP), caspase activation to cleave hundreds of proteins, DNA fragmentation, and blocked translation. Little is known about the fate of RNA as cells die, even though apoptosis has been intensively studied for decades. Here I show that mRNAs, but not noncoding RNAs (ncRNAs), are rapidly and globally degraded during apoptosis. The decay occurs in many cell types responding to diverse apoptotic stimuli. mRNA decay is triggered early in apoptosis, preceding membrane lipid scrambling, genomic DNA fragmentation and modifications to translation initiation factors that might cause translational arrest. mRNA decay depends on MOMP and is amplified by effector caspase activity. 3' truncated mRNA decay intermediates with nontemplated uridylate-rich tails are generated during apoptosis and degraded by the 3' to 5' exonuclease DIS3L2. Knockdown of DIS3L2 reduces apoptotic mRNA decay and partially rescues cell death. I propose that global mRNA decay is a new hallmark of apoptosis caused by the concerted action of several nucleases.
I also report a new role for RNA and DNA in directing cytotoxic leukocyte proteases to their substrates. When cytotoxic lymphocytes recognize and attack infected or cancerous cells, they deliver the granzyme (Gzm) serine proteases into the target cell. The Gzms cleave diverse protein substrates to orchestrate cell death. RNA binding proteins are highly enriched in unbiased proteomic screens of Gzm protein substrates. I hypothesized that the Gzms are guided to nucleic acid binding protein targets via direct binding to RNA or DNA. Using fluorescence polarization, I show that the Gzms and related leukocyte proteases bind to RNA and DNA with low nanomolar affinity. Nucleic acid binding by the Gzms facilitates their cleavage of RNA and DNA binding proteins, and guides them into target cell nuclei and onto neutrophil extracellular traps. Nucleic acid binding provides an elegant mechanism to confer protease substrate specificity for cleavage of nucleic acid-binding proteins that play essential roles in cellular gene expression and cell proliferation.
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Chang, Howard Y. (Howard Yuan-Hao) 1972. "Molecular studies of Fas signaling and programmed cell death". Thesis, Massachusetts Institute of Technology, 1998. http://hdl.handle.net/1721.1/50483.
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Agapite, Julie 1968. "Genetic analysis of programmed cell death in Drosophila melanogaster". Thesis, Massachusetts Institute of Technology, 2002. http://hdl.handle.net/1721.1/8321.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2002.Includes bibliographical references.
The correct regulation of programmed cell death, or apoptosis, is critical for proper development and prevention of disease. Components of the molecular mechanisms that govern apoptosis are conserved among organisms as diverse as C. elegans, Drosophila, and mammals. A central step in the execution of cell death is the activation of caspases, a conserved family of cysteine proteases. In Drosophila, the proteins, Reaper (Rpr), Head involution defective (Hid), and Grim, induce cell death via a mechanism that involves caspase activation. In order to further elucidate the mechanisms underlying the control of apoptosis, we conducted screens for genes involved in Rpr- or Hid-induced cell death. The analysis of the mutants isolated led to several new insights. The death inducing activity of Hid is post-transcriptionally down-regulated by the Ras/MAPK pathway. This is consistent with the pro-survival activity of this pathway and is probably mediated by direct phosphorylation of Hid. Furthermore, analysis of mutations in the gene encoding the Drosophila IAP, Diapl, led to a model for how Rpr, Hid and Grim activate caspases and induce cell death. In this model, Diapl binds and inhibits caspases; Rpr, Hid, and Grim induce cell death by binding Diapl and relieving caspases of Diapl-mediated inhibition. In addition, our mutants indicate that Diapl's RING finger domain, a domain found in proteins that function in ubiquitination, is required for inhibition of Rpr- and Grim-induced death but not Hid-induced death.
(cont.) Moreover, we identified a predicted ubiquitin conjugating enzyme, dBRUCE, which also functions to inhibit Rpr and Grim but not Hid. We propose that Diapl and dBRUCE function together to inhibit Rpr- and Grim-induced death by ubiquitinating pro-apoptotic proteins, possibly caspases or Rpr and Grim themselves, and targeting them for degradation by the proteasome. These findings are likely applicable to mammalian systems, since both dBRUCE and Diapl are conserved proteins with close homologs in murine and human genomes.
by Julie Agapite.
Ph.D.
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Gao, Zhonghua. "Regulation of the molecular machinery of programmed cell death /". Access full-text from WCMC, 2009. http://proquest.umi.com/pqdweb?did=1619236691&sid=11&Fmt=2&clientId=8424&RQT=309&VName=PQD.
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RUNYAN, CHRISTOPHER MICHAEL. "The Role of Cell Death in Germ Cell Migration". University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1210732680.
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King, Andrea Rebecca. "The genetic control of programmed cell death (apoptosis) in human endothelial cells". Thesis, University of Sheffield, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310942.
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Young, Bennett. "Is the Arabidopsis peptide 'kiss of death' an inducer of programmed cell death?" Thesis, University of Manchester, 2010. https://www.research.manchester.ac.uk/portal/en/theses/is-the-arabidopsis-peptide-kiss-of-death-an-inducer-of-programmed-cell-death(33ac50ec-bd4f-4069-8618-bcd21e520b23).html.
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Programmed Cell Death (PCD) is an essential process utilised for the defence and development of all multicellular organisms. In plants however, relatively little is known about the genes involved with the regulation and execution of this process. In particular, even less is known about the molecular components which act high up in the PCD pathway. In this thesis, we carried out an investigation into the novel peptide-encoding gene KISS OF DEATH (KOD). In Arabidopsis, KOD was found to be involved with mediating the elimination of the suspensor, an organ which undergoes developmental PCD. Two mutant alleles of KOD showed reduced PCD in both the suspensor and during heat-shock induced PCD of root hairs. Over-expression of KOD in plant tissues was sufficient to cause death in leaves or whole seedlings and involved the activation of caspase-like proteolytic activity. KOD-induced PCD was found to require light in leaves and is also sensitive to the PCD suppressor genes AtBI-1 and P35. We suggest that KOD acts high up in the PCD cascade as its expression resulted in depolarisation of the mitochondrial membrane, which is an early step in plant PCD. KOD appears to be a plant-specific peptide that is sufficient to induce PCD in Arabidopsis in the absence of external triggers. Typical BLAST searches yielded no obvious homolog for KOD, therefore a bioinformatics screen of the Arabidopsis genome was carried out. This screen for small genes similar in size to KOD enabled us to detect 10 previously unidentified genes, one of which may represent a putative KOD homolog. In summary, KOD appears to be a novel pro-PCD component of the Arabidopsis cell death machinery and represents the first plant peptide to be involved with a form of developmental PCD.
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Roche, Meghan C. "A study of programmed cell death in cotton (gosypium hirsutum) fiber". Thesis, [College Station, Tex. : Texas A&M University, 2007. http://hdl.handle.net/1969.1/ETD-TAMU-1599.
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Monetti, Emanuela. "Role of ion channels in programmed cell death induced by hyperosmotic stresses in plant cells". Thesis, Paris 11, 2014. http://www.theses.fr/2014PA112323/document.
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Le travaux présenté dans cette thèse concerne le rôle des canaux ioniques de la membrane plasmique en réponse à des stress salins et non salins ainsi qu’aux interactions possibles avec d’autres événements de signalisation conduisant à la mort cellulaire programmée (PCD). Nous avons montré que les réponses cellulaires précoces: tels que l`augmentation du calcium cytosolique et la production de ROS, classiquement impliqués lors de la PCD, ne semblaient pas être impliqué dans la mort cellulaire induite par les stress hyperosmotiques chez les cellules en culture de tabacco BY2 ou d’A. thaliana. Nous avons montré que, dans les cas de stress salin chez les cellules de BY2 un influx précoce de sodium à travers des canaux cationiques non spécifiques participe au développement de la PCD en entraînant un disfonctionement mitochondrial et la production de O2• - par des NADPH oxydases. Dans le cas de stress hyperosmotique non-ionique, nous avons observé une diminaution précoce de l’intensité des courants anioniques. Afin de poursuivre l’étude du rôle des canaux anioniques lors du stress hyperosmotique non salin, nous avons utilisé des cellules A.thaliana nous permettant de travailler avec le mutant de canal anionique SLAC1. Nous avons constaté que l’activation retardée des canaux SLAC1 participait au développement de la PCD induite par un stress hyperosmotique non salin. La réduction précoce de l'activité des canaux anioniques pourrait participer à la signalisation ou l'ajustement osmotique permettant l'adaptation et la survie cellulaire alors que des évènements retardés, à savoir la production d'anion superoxyde (O2• -) par les NADPH-oxydases et l'activation des canaux anioniques pourraient participer au développement de la PCD d'une partie de la population cellulaire. Nous avons aussi étudié le rôle potentiel des petits peptides appartenant à la famille des peptides FMRFamide décrite chez les métazoaires à l'osmorégulation chez des cellules d’A. thaliana. Des génes susceptibles de coder de tels peptides sont en effet présent dans le génome d’A. thaliana. En utilisant des peptides synthétiques, nous avons montré que ces FLPS putatifs pourraient participer aux réponses induites losr de stress hyperosmotique chez les plantes. Ce travail illustre la complexité et l'importance de la régulation des canaux ioniques dans les voies de signalisation et les processus conduisant à la PCDThe work presented in the present thesis relates to the role of ion channels in response to (ionic and non-ionic) hyperosmotic stresses and their interactions with signaling events leading to PCD in plant. Early cell responses such as cytosolic calcium increase and ROS production classically involved in PCD process, seems not to be involved in hyperosmotic-induced cell death in BY2 tobacco and A. thaliana cultured cells. When BY2 tobacco cells were subjected to hyperosmotic stress, an early influx of sodium through non-selective cation channels participates in the development of PCD through mitochondrial dysfunction and NADPH-oxidase-dependent O2•– generation. On the contrary, non-ionic hyperosmotic stress resulted in an early decrease in anion currents. To further investigate the role of anion channels in non-ionic hyperosmotic stress further experiments were conducted by using A.thaliana cells of the anion channel mutant SLAC1. Results showed that the delayed activation of SLAC1 channels was involved in the non-ionic hyperosmotic stress induced pathway leading to cell death. Interestingly, the early anion channel activity decrease could participate to signalisation or osmotic adjustment allowing cell adaptation and survival, when a second set of events, namely superoxide anion (O2•-) generation by NADPH-oxidase and anion channel activation could participate in PCD development of a part of the cell population. In addition, the potential role of small peptides belonging to the FMRFamide-like peptide (FLP) family described in metazoan in osmoregulation in A. thaliana was investigated. By using synthetic peptides, based on FLPs homolog genes existing in A. thaliana, it was possible to demonstrate that these putative FLPs are involved in hyperosmotic stress response. Overall, the present work shed light on the importance and the complexity of ion channels regulation in the signaling pathways and the processes leading to PCD
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Jones, Nicola L. "Microbial induction of programmed cell death in the gastrointestinal tract". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0017/NQ45750.pdf.
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Anwar, Khurshid. "Role of apoptosis (programmed cell death) in acute liver failure". Thesis, University of Surrey, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370058.
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Johnsen, Holly L. (Holly Louise). "Studies of programmed cell death in the nematode caenorhabditis elegans". Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/104115.
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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2016.This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student-submitted PDF version of thesis.
Includes bibliographical references.
Programmed cell death is an evolutionarily conserved process that plays critical roles in normal animal development and has been extensively studied in C. elegans. During programmed cell death, caspases are activated in the dying cell. The cell corpse is engulfed by a neighboring cell and degraded. Almost all cell deaths in C. elegans are "suicides"-they are caspase-dependent and apparently cell-autonomous, and do not require engulfment. During development of the C. elegans male, the cells B.alapaav and B.arapaav are generated during the late third-larval stage. During the early fourth-larval stage one of these cells undergoes programmed cell death, and the other survives. These two cells form an equivalence group; the decision of which cell dies and which survives is stochastic. The cell that dies is engulfed by the neighboring cell P12.pa and was speculated to be an engulfment-dependent cell "murder" or an "induced suicide." I have discovered that B.al/rapaav instead represents an "assisted suicide" that requires both the core apoptosis pathway and the engulfment pathway. egl-1 and ced-3 are expressed in the dying or undead cell in wild-type and engulfment-defective animals, and these genes are required for the B.al/rapaav cell death. In engulfment mutants the B.al/rapaav death process fails at a point after caspase activation, suggesting that the core cell-death pathway is necessary but not sufficient for this cell death. Previous genetic screens have not been designed to systematically identify essential genes with a role in cell death. Most somatic cell deaths in C. elegans occur during early development, but several male-specific cell deaths occur during the fourth larval stage. These late cell deaths provide an opportunity to examine essential genes for a role in programmed cell death, as RNAi treatment after hatching can eliminate gene function before these deaths occur but after embryogenesis. I performed an RNAi screen for 1,132 essential genes and assayed the effect on Rn.aap cell survival. I analyzed candidate genes for non-specific effects, such as affecting the Rn cell lineage rather than cell death processes, to find twenty-five essential genes that might have a role in the Rn.aap cell death.
by Holly L. Johnsen.
Ph. D.
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Silva, Thiago Pereira da. "Bacteria from freshwater ecosystems: structural aspects and programmed cell death". Universidade Federal de Juiz de Fora (UFJF), 2017. https://repositorio.ufjf.br/jspui/handle/ufjf/6145.
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Bacteria are important components of the food web structure in aquatic ecosystems in which they influence the flow of carbon and energy. Populations of bacteria in these ecosystems comprise a diverse spectrum of individual cells able to respond to many factors such as nutrient supply, temperature and virus infection, which regulate bacterial life and death. Bacterial death is a key cellular event involved in the control and production of bacteria in aquatic ecosystems with functional meaning in the carbon and nutrient cycles. Therefore, the study of bacterial structural features and cellular mechanisms underlying bacterial death is crucial to understand processes affecting the entire population. However, both bacterial structure and cellular events of death in aquatic ecosystems are still poorly understood. In the present work, we used single cell approaches to study the structural organization of bacteria as well as to characterize cellular processes of death in these organisms. First, by using fluorescence and transmission electron microscopy (TEM), we provided a general panorama of how microscopy techniques, especially TEM, are powerful tools to understand bacterial structure and their responses to environmental stresses. We showed that bacteria from aquatic ecosystems have remarkable ultrastrutural diversity with components such as bacterial envelope of individual cells differing in structure within the same population. Second, we sought to identify and characterize mechanisms of bacterial cell death. Because our TEM analyses revealed morphological signs of apoptosis, a type of program cell death (PCD), in aquatic bacteria directly collected from natural ecosystems, we applied different techniques to detect apoptosis in bacteria cultured from natural samples. We used TEM as well as different probes to detect this type of PCD in cultured bacteria exposed to increased temperature and viral infection, which are recognized inducers of bacterial death. TEM showed, in both situations, ultrastructural changes indicative of apoptosis, such as cell retraction and condensation, similar to those reported for eukaryotic cells. Assays for membrane permeability, DNA fragmentation, phosphatidilserine exposition and caspase activation were significantly increased in treated bacteria compared to the control group. Altogether, our data demonstrate, for the first time, that PCD occur in aquatic bacteria, and that this event may be a basic mechanism for regulation of bacterial communities in these ecosystems.
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Caballero, Ramon Edwin. "Selective Induction of Programmed-cell Death in HIV-infected Macrophages". Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37650.
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In order to achieve cure for HIV-1 infection in patients undergoing suppressive antiretroviral therapy, eradication of all latently infected reservoirs of the virus is required. The focus of HIV cure is predominantly centred on the elimination of latently infected memory T cells, while information on possible elimination of infected macrophages is lacking. Macrophages support continuous virus replication without succumbing to cytopathic effects of HIV-1. Recently, our laboratory has shown a protective role for cellular inhibitor of apoptosis proteins (IAPs) 1/2 in macrophages against Vpr-induced apoptosis. Depletion of cIAP1/2 by Smac mimetics (SM) reverse the IAP-mediated protection and sensitize macrophages to Vpr-induced cell death. My research aims to understand the role IAPs play in apoptotic resistance of HIV-infected macrophages. I hypothesized that ablation of cIAP1/2 by SM may induce apoptosis in HIV-infected macrophages. My results show that SM does not induce cell death in uninfected or healthy macrophages, but induces cell death in chronically infected U1 cells, in vitro infected monocyte-derived macrophages, and ex vivo derived HIV-infected macrophages from HIV-infected individuals. SM induce cell death of infected myeloid cells through apoptosis and not through necroptosis. Moreover, SM-induced apoptosis is independent of TNFα and other endogenously secreted cytokines. In vitro infection of monocyte-derived macrophages leads to the downregulation of RIPK1, RIPK3, and TRAF-1. Interestingly, necrostatin-1-mediated RIPK1- inhibition does not affect viability of healthy macrophages, but in combination with IAP degradation by SM leads to significant induction of apoptosis. This suggests a key role for RIPK1 in SM-induced apoptosis of HIV-infected macrophages. Altogether, the results from this project suggest that modulation of the IAP-associated signalling pathways by SM may be a potential strategy for selective killing of HIV-infected macrophages.
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Blaschke-Bonkowsky, Anne Jeannette. "Programmed cell death during embyronic development of the mammalian CNS /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1997. http://wwwlib.umi.com/cr/ucsd/fullcit?p9805793.
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Tan, Shirlee W. "Oxidative glutamate toxicity : an unusual form of programmed cell death /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1999. http://wwwlib.umi.com/cr/ucsd/fullcit?p9956464.
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Brand, Verena Beatrice. "Programmed cell death in Plasmodium infected normal and sickle trait red blood cells". [S.l. : s.n.], 2007.
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Winbush, Ari. "Steroid-triggered, cell-autonomous programmed cell death of identified Drosophila motoneurons during metamorphosis /". Connect to title online (Scholars' Bank) Connect to title online (ProQuest), 2008. http://hdl.handle.net/1794/9503.
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Winbush, Ari 1979. "Steroid-triggered, cell-autonomous programmed cell death of identified Drosophila motoneurons during metamorphosis". Thesis, University of Oregon, 2008. http://hdl.handle.net/1794/9503.
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x, 83 p. : ill. (some col.) A print copy of this thesis is available through the UO Libraries. Search the library catalog for the location and call number.Programmed cell death (PCD) is a critical process during development and maturity of vertebrates and invertebrates. Aberrations in PCD are responsible for numerous developmental abnormalities and diseases in humans. Cell death pathways are surprisingly similar across species, so the study of PCD in simpler organisms such as insects provides important insight into the roles of cell death in higher animals including humans. Metamorphosis of the fruit fly, Drosophila melanogaster , provides an excellent model system in which to study PCD. During metamorphosis, many obsolete larval structures undergo PCD, largely in response to changes in circulating levels of steroid hormones known as ecdysteroids. These effects of ecdysteroids are particularly striking in the nervous system, where many larval neurons undergo PCD or functional remodeling during metamorphosis. One wave of neuronal PCD takes place during the first 24 hours of metamorphosis while a second follows adult emergence. Studies in another insect, Manduca sexta , suggested that the rise in ecdysteroids that initiates metamorphosis, the prepupal pulse, may trigger the first wave of neuronal PCD in Drosophila . This dissertation investigated steroid-regulated neuronal PCD in Drosophila by studying an individually-identified larval motoneuron, RP2. Using molecular genetics, ïmmunocytochemistry and primary cell culture, I showed that abdominal RP2s undergo PCD within the first 24 hours of Drosophila metamorphosis; identified a role for previously-identified PCD genes and ecdysteroid receptors in RP2's demise; and demonstrated that the prepupal pulse of ecdysteroids acts directly and cell-autonomously on RP2s to activate PCD. These experiments advance our understanding of hormonally-induced cell death and its regulation within the developing nervous system. This dissertation includes unpublished co-authored material.
Adviser: Janis C. Weeks
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Gough, Julie. "Apoptosis of human osteoblasts cultured on polymeric biomaterials in vitro". Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298960.
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Molostvov, Guerman. "Regulation of endothelial cell apoptosis and its role it the pathogenesis of HUS and multiple myeloma". Thesis, University of Warwick, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269536.
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James, Claerwen Laura. "Analysis of components of the Caenorhabditis elegans cell death apparatus in a heterologous system". Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300783.
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Zeng, Lirong. "A novel mechanism underlying programmed cell death in plant defense signaling". Connect to resource, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1120255271.
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Harvey, Jagger J. W. "Investigations into the nature and regulation of plant programmed cell death /". For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2005. http://uclibs.org/PID/11984.
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Nandy, Anubhab. "The Role of NFκB Factor Relish in Developmentally Programmed Cell Death". eScholarship@UMMS, 2018. https://escholarship.umassmed.edu/gsbs_diss/956.
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Several types of cell death including apoptosis, necroptosis and autophagic cell death play diverse roles in different biological processes. In addition to its essential roles in development and metabolism, programmed cell death is indispensable for host immunity. Interestingly, current research shows that these processes are connected but the nature and extent of the crosstalk between host defense and programmed cell death still remains an area of great interest.
The NFkB factor Relish is best characterized as a crucial component of Drosophila Imd pathway, which generates immune responses by producing antimicrobial peptides following Gram-negative bacterial infection. In this dissertation, I demonstrate a novel role of Relish in developmentally programmed cell death. During metamorphosis, Drosophila salivary glands are degraded by the collective actions of caspase-dependent and autophagic cell death. Here I show that Relish mutants displayed improper salivary gland degradation and the persistence of salivary gland cell fragments. Expression of Relish in salivary glands rescued this phenomenon. Among the upstream components of the Imd pathway, mutants in the bacterial peptidoglycan receptors, PGRP-LC and-LE also exhibited similar defects in gland degradation, but surprisingly none of the other Imd pathway components examined had any such effect. As both Relish and PGRPs are critical for host defense against bacterial infection, our next concern was the role of host microflora in salivary gland degradation. However, observation of normal salivary gland cell death in axenic flies ruled out the possible involvement of microbiota. Robust genetic analyses proved that Relish-mediated cell death occurs in caspase-independent but autophagy-dependent manner. Moreover, expressions of either active version of Relish or PGRP-LC resulted in the premature gland degradation and induction of autophagy. Finally, I show that Relish controls autophagy by regulating the expression of Atg1, a core component of the autophagy pathway. Together these findings suggest the existence of a novel pathway, which connects immune response factors to developmentally programmed cell death.
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Sobhani, Kimia. "Proteomic analysis of macrophage proinflammatory programmed cell death and macrophage activation /". Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/8688.
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Galvin, Brendan D. (Brendan Daniel). "The regulation of programmed and pathological cell death in C. elegans". Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/38633.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, February 2007.Includes bibliographical references.
Programmed cell death, or apoptosis, is important in the development and homeostasis of metazoans. In the nematode C. elegans, four genes, egl-1, ced-9, ced-4, and ced-3, constitute the core pathway acting in all somatic programmed cell deaths. This pathway is evolutionarily conserved in humans. The BH3-only protein EGL-1 is transcriptionally upregulated in cells fated to undergo programmed cell death, and EGL-1 blocks cell-death inhibition by the cell-death regulator CED-9, a Bcl-2 family member. The binding of EGL- 1 to CED-9 releases the Apaf- 1-like adaptor protein CED-4 from CED-9, so that CED-4 can activate the caspase CED-3, a protease that is the effector of programmed cell death. In this thesis, I describe three projects, each of which examines one aspect of C. elegans cell death. From. screens for mutations that increase cell death in a sensitized genetic background, I identified a gene that protects cells from programmed cell death.
(cont.) This gene, spk-1, encodes a homolog of SR protein kinases, which regulate alternative splicing. Previous work has shown that ced-4 pre-mRNA is alternatively spliced to generate two transcripts that function oppositely in cell death. I found that spk-1 regulates ced-4 transcript splicing, thereby influencing the amount of programmed cell death that occurs. From a screen for genes that promote programmed cell death, I isolated a mutation in a conserved non-coding element in the transcriptionally regulated cell-death activator gene egl-1. This element regulates the deaths of specific cells in the C. elegans ventral nervous system. I found a novel C. elegans transcription factor, Y38C9A. 1, that binds this element and might function to regulate egl-1 transcription and programmed cell death in the ventral nervous system. In addition to the programmed cell deaths that occur in C. elegans, pathological death of specific cells can be caused by mutations in some genes. I characterized two genes, lin-24 and lin-33, that can mutate to cause the inappropriate death of specific hypodermal blast cells. One of these genes, lin-24, contains a domain similar to that found in some bacterial toxins.
(cont.) By morphological and genetic criteria, I show that the lin-24- and lin-33-mediated deaths are unlike previously characterized necrotic and apoptotic cell deaths in C. elegans. These deaths require some of the genes responsible for engulfing the corpses generated by programmed cell death, even though the deaths do not require the core genes of the genetic pathway of programmed cell death.
by Brendan D. Galvin.
Ph.D.
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Ingram, Justin Phillip. "The Role of the Innate Immune System in Programmed Cell Death". Diss., Temple University Libraries, 2018. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/516594.
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Biomedical SciencesPh.D.
Infectious diseases are the leading cause of illness worldwide, leading to over 20 million hospitalizations each year in the United States alone. Although numerous diseases are treatable with vaccines and pharmacological agents, including antibiotics, a large fraction of infections remain poorly controlled, mainly due to lack of effective therapies and/or vaccines. Two such infectious agents are influenza A virus and the bacterium Salmonella enterica. Influenza A virus is transmitted through the aerosol route and infects lung epithelial cells, while Salmonella is transmitted via the fecal-oral route and infects the cells lining the intestine of the host. In each case, the first lines of defense against these infectious agents are non-phagocytic cells. How these pathogens are controlled in non-phagocytic cells dictates the overall outcome of infection; however there are significant gaps in our knowledge of how non-phagocytic cells respond to influenza A virus and Salmonella. Therefore, studying the fate of these cells during the course of infection is of crucial importance to disease outcome. In each case, the regulated (or programmed) death of the infected cell may represent an important pathogen clearance mechanism. Programmed cell death can be non-inflammatory (e.g., apoptosis) or pro-inflammatory (e.g., necroptosis and pyroptosis). In this dissertation, I outline experiments carried out to identify the pathways of programmed cell death activated by Salmonella and influenza A virus in their respective target non-phagocytic cells, both in vitro and in vivo. My work outlines new pathways of cell death activated by these pathogens and new mechanisms of both viral and bacterial clearance. This will have broad implications in the clearance of pathogens, and new therapeutic avenues to pursue upon treating infections.
Temple University--Theses
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Back, Chelsea. "Induction of programmed cell death in mammalian cells by isolates of Ross River virus". Thesis, Back, Chelsea (2011) Induction of programmed cell death in mammalian cells by isolates of Ross River virus. Honours thesis, Murdoch University, 2011. https://researchrepository.murdoch.edu.au/id/eprint/11832/.
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Arthritogenic alphaviruses, such as Ross River virus (RRV) are associated with worldwide outbreaks of human polyarthritis/arthralgia. The pathogenesis of RRV and other alphaviruses is poorly understood. Studies have shown potential links between the different strains of RRV and variation in their pathogenesis and virulence. Currently there is believed to be two circulating strains of RRV, the south western (SW) from the south west region of Western Australia and the north eastern (NE) from the east coast of Australia. Studies have suggested that the persistence of RRV may be the result of an impaired immune response. This study was designed to determine if the SW and NE isolates of RRV have the ability to induce apoptosis in DCs and fibroblasts and discover any possible variation in their apoptosis-inducing capacity. Both Vero cells and murine bone marrow DCs (BMDCs) were infected with the SW74249 (SW) and SW82627 (NE) strains of RRV. A time course analysis of two apoptotic markers and a cell viability marker for both cell types was conducted by flow cytometry. The results indicate RRV- induced apoptosis in both Vero cells and BMDCs, with RRV inducing a stronger pro-apoptotic response in BMDCs than Vero cells, 24 h after infection. Between the two strains there was little variation in the Vero cells over time. In the BMDCs there was some variation with the RRV-SW strain inducing a higher percentage of cell death than the RRV-NE strain, 24 h after infection. Collectively, the data indicates that RRV has the capacity to induce a pro-apoptotic response in DCs, with the SW presenting as more aggressive compared to the NE, potentially leading to greater virulence. This data could help to explain the mechanism of RRV persistence in vertebrate hosts, as well as the reported differences in severity and duration of human clinical symptoms. Immunotherapy aimed at correcting the patient’s dysfunctional immune system, may represent a new strategy for the successful medical treatment of RRV infection.
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Orchard, Craig Brailsford. "Relationship between programmed cell death and the cell cycle in the tobacco BY-2 cell line". Thesis, Cardiff University, 2004. http://orca.cf.ac.uk/55931/.
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Ethylene is an established plant growth regulator linked with programmed cell death (PCD). To investigate the relationship between the cell cycle and PCD, ethylene was used to see if it induced mortality in a cell cycle specific manner. Tobacco BY-2 cultures synchronized with aphidicolin were treated with ethylene. Cell cycle progression and mortality, measured at hourly intervals, showed distinct peaks of mortality at the G2/M boundary and S-phase. In conjunction with this, DNA fragmentation increased at G2/M. Furthermore, ethylene caused a significant reduction in cell size of the cycling population. Simultaneous addition of silver nitrate with ethylene ameliorated ethylene-induced G2/M mortality, although a toxic effect of silver alone was evident. Due to the toxicity of silver, 1-MCP, an alternative chemical for blocking ethylene receptors was used. 1-MCP neither affected the BY-2 cell cycle nor mortality levels. In addition, 1-MCP ameliorated ethylene-induced G2/M mortality. To balance the chemical approaches to blocking ethylene receptors, tobacco BY-2 cells were transformed with Atetrl that encodes a dominant insensitive form of the Arabidopsis ETR1 ethylene receptor. Atetrl expression caused a massive perturbation to the tobacco BY-2 cell cycle, especially in S-phase, and resulted in high levels of mortality throughout the cell cycle. Ethylene treatment caused a doubling of G2 duration but did not affect temporal distribution of mortality. However, ethylene treatment generated a peak of mortality in S-phase. These results suggest that ethylene induces PCD at G2/M through the known ethylene signaling pathway. Furthermore, it confirms that 1-MCP and Atetrl result in ethylene insensitivity. To examine the G2/M transition, Spcdc25, a positive regulator of G2/M in fission yeast was transformed into the tobacco BY-2 cell line. This resulted in premature entry into mitosis, a shortened cell cycle, and reduced cell size. This was similar to Spcdc25 over-expression in fission yeast and suggests the presence of a CDC25-like phosphatase in plants.
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Zheng, A. (Aiping). "All-trans retinoic acid-induced apoptosis in acute myeloblastic leukemia cells:with a special emphasis on p53, Bcl-2, and mitochondria". Doctoral thesis, Oulun yliopisto, 2000. http://urn.fi/urn:isbn:9514256735.
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Abstract
All-trans retinoic acid (ATRA) is a derivative of vitamin A. It is able to stimulate neutrophilic differentiation of normal progenitors and acute promyelocytic leukemia (APL) cells. Although ATRA-induced differentiation is not observed in any other acute myeloblastic leukemia (AML) subtypes, ATRA is known to be able to inhibit AML blast cell proliferation. The present in vitro study using AML cell lines representing subtypes other than APL focuses on the following questions: (1) Is the inhibitory effect of ATRA on AML cell growth related to apoptosis of cells? (2) Are the effects of ATRA dependent on two important regulators of apoptosis, p53 and Bcl-2? (3) Do mitochondria have any role in mediating the effects of ATRA? ATRA-induced apoptosis in AML cells was observed by morphology, DNA fragmentation, phosphatidylserine externalization, and poly(ADPribose)polymerase (PARP) cleavage. It was a slow event, manifested as DNA cleavage after 48 hours exposure and as morphological apoptosis after 72 hours exposure. The AML cells expressed constitutively p53 as determined by immunohistochemistry, Western blotting and flow cytometry. However, no mutation of TP53 was observed in exons 5 to 8 as analysed with a single strand conformation polymorphism technique. As the flow cytometer analysis showed, most of p53 was in a aberrant conformation, which was not changed into a wild type conformation by ATRA. Two of the cell lines were analysed more specifically in relation to Bcl-2 and mitochondral function: ATRA-induced apoptosis of the cell lines was associated with down-regulation of Bcl-2. Western blotting showed ATRA-induced apoptosis also to be related to the release of cytochrome c from mitochondria into cytosol, resulting in the activation of caspase-3, an apoptotic effector, which was manifested as a cleavage of its substrate PARP. The process was also accompanied by disruption of the mitochondrial membrane potential as determined fluoricytometrically. These results show that ATRA is able to induce apoptosis in AML cells other than APL, and ATRA-induced apoptosis in the AML cells studied is related to the down-regulation of Bcl-2 and the disruption of mitochondrial function, but is independent of the p53 pathway.
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Calver, Andrew Robert. "Oligodendrocyte population dynamics : insights from transgenic mice". Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322239.
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Metzstein, Mark M. (Mark Mordecai) 1969. "Analysis of genes involved in cell-specific control of programmed cell death in Caenorhabditis elegans". Thesis, Massachusetts Institute of Technology, 1998. http://hdl.handle.net/1721.1/9661.
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Thesis (Ph.D.)--Massachusetts Institute of Technology, Dept. of Biology, 1999.Includes bibliographical references.
Programmed cell death is an important process regulating cell number in the development of all animals. Two genes, ces-1 and ces-2 control programmed cell death in a subset of developing neurons in C. elegans. To understand how ces-1 and ces-2 might act to regulate programmed cell death, we have cloned these genes. We find that both ces-1 and ces-2 encode transcription factors. By sequence and DNA-binding specificity CES-1 is a member of the Snail family of zinc-finger proteins, and most similar to the Drosophila protein Scratch. CES-2 is a bZIP protein closest in sequence and DNA-binding specificity to members of the vertebrate PAR subfamily. We have analyzed ces-1 regulation and, by conservation in the related nematode C. briggsae and by the position of the ces-1 gain-of-function mutations, identified a putative control element 5' of ces-1 coding sequences. This element contains a site that can be bound by CES-2 protein, suggesting ces-1 may be transcriptionally regulated directly by ces-2. This element also contains five Snail-like binding sites, suggesting ces-1 may regulate its own transcription. These results suggest that programmed cell death, like many cell fates, is under transcriptional control, and that a transcriptional cascade control the deaths of at least some cells in C. elegans. We propose that some of the ced genes, which are involved in the execution of programmed cell death in C.elegans, are transcriptionally regulated by CES-1 and/or CES-2. Additionally, both ces-1 and ces-2 have homologues which might function in regulating programmed cell death in mammalian cells, suggesting the functions of ces-1 and ces-2 may be evolutionarily conserved.
by Mark M. Metzstein.
Ph.D.
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Driscoll, Kaitlin B. (Kaitlin Bridget). "Genetic and molecular studies of cell-autonomous execution during programmed cell death in C. elegans". Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/104177.
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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2016.Cataloged from PDF version of thesis.
Includes bibliographical references.
Apoptosis or programmed cell death was originally defined by evolutionarily conserved morphological characteristics that include shrinkage of cell volume and chromatin condensation. Apoptosis functions as a highly controlled mechanism for the elimination of unwanted or damaged cells and is essential for disease prevention. Apoptotic cell death is a cell-autonomous process driven by the caspase family of cysteine proteases. The discovery of the CED-3 caspase in C. elegans led to the paradigm that caspase cleavage of substrates drives cell death and promotes engulfment. While many caspase substrates have been identified, it is not well understood how caspase substrates act to promote cell death and engulfment. The control of caspase activation in C. elegans is conserved among metazoans and involves the interplay of pro and anti-apoptotic BCL-2 and BH3-only family proteins. In C. elegans an increase in apoptotic cell refractility observed by Nomarski optics is one of the hallmark morphological characteristics of apoptosis. We found that the presumptive TRP channel CED-1 1 acts downstream of caspase activation in apoptotic cells to drive the increase in refractility. We discovered that CED-1 1 is also required for a decrease in cell volume and increase in nuclear permeability of apoptotic cells. We showed that CED-1 1 is required for efficient degradation of apoptotic cells and facilitates the death process, suggesting that the decrease in cell volume and/or increase in nuclear permeability could promote the death and degradation of the cell. We conclude that CED-1 1 acts downstream of caspase activation to effect multiple observed changes to apoptotic cells and to facilitate death and degradation. In addition we investigated the anti-apoptotic function of the generally pro-apoptotic BCL-2 homolog CED-9.
by Kaitlin B. Driscoll.
Ph. D.
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Shi, Yuquan Shi Yu-Quan. "Studies of programmed cell death and genetic instability induced by X-rays /". [S.l.] : [s.n.], 2000. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=13701.
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Huang, Shuanglong. "Mechanisms of programmed cell death modulated by phytoglobins in maize somatic embryogenesis". American Society of Plant Biologists, 2014. http://hdl.handle.net/1993/30312.
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Hemoglobins (Hbs) are heme-containing proteins belonging to the globin superfamily that are ubiquitous in most living organisms including prokaryotes and eukaryotes. In addition to the first legHbs found in leguminous plants, there are another three classes of phytoglobins (Pgbs) identified in various plant species including dicots and monocots. The ability of heme groups to bind gaseous ligands such as oxygen, carbon monoxide and nitric oxide (NO) places Pgbs as multifunctional players in various processes during plant growth and development under normal or stress conditions. The objective of this project is to investigate how transcriptional manipulation of ZmPgb1.1 and ZmPgb1.2 influences somatic embryogenesis in maize (Zea mays). Suppression of either of the two genes is sufficient to induce programmed cell death (PCD) through a pathway initiated by accumulation of nitric oxide (NO) and zinc (Zn2+), and mediated by production of reactive oxygen species (ROS). The effect of the death program on the fate of the developing embryos is dependent upon the localization patterns of the two Pgbs. During somatic embryogenesis, ZmPgb1.2 transcripts are restricted to a few cells anchoring the embryos to the subtending embryogenic tissue, while ZmPgb1.1 transcripts extend to several embryonic domains. Suppression of ZmPgb1.2 induces PCD in the anchoring cells allowing the embryos to develop further, while suppression of ZmPgb1.1 results in massive PCD leading to embryo abortion. Cells suppressing the Pgb genes are also depleted of endogenous auxin (indole-3-acetic acid, IAA) localization established by polar auxin transport (PAT), thus suggesting a possible involvement of this plant hormone in the observed processes. Collectively, it appears that the cell specific expression of Pgbs has the capability to determine the developmental fate of embryogenic tissue during maize somatic embryogenesis through their effect on PCD. This novel regulation has implications for development and differentiation in other species.
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Jones, Helen Elizabeth. "Programmed cell death in the larval salivary glands of the Drosophila melanogaster". Thesis, Cardiff University, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.304855.
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