Tesi sul 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.
Testo completoOron 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.
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.
Testo completoSharma, 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.
Testo completoPalazzo, 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.
Testo completoWilkinson, Derek. "Proteases and programmed cell death in fungi". Thesis, University of Exeter, 2011. http://hdl.handle.net/10036/3629.
Testo completoJagasia, Ravi. "Mitochondrial dynamics in Caenorhabditis elegans programmed cell death". Diss., [S.l.] : [s.n.], 2005. http://edoc.ub.uni-muenchen.de/archive/00004281.
Testo completoCowling, 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.
Testo completoDrury, 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.
Testo completoCameron, Angus Crawford. "The control of physiological programmed cell death : apoptosis". Thesis, The University of Sydney, 1991. http://hdl.handle.net/2123/4751.
Testo completoNelson, Charles J. "MicroRNA Regulation of Autophagy during Programmed Cell Death: A Dissertation". eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/756.
Testo completoNelson, Charles J. "MicroRNA Regulation of Autophagy during Programmed Cell Death: A Dissertation". eScholarship@UMMS, 2003. http://escholarship.umassmed.edu/gsbs_diss/756.
Testo completoAsavaritikrai, Pundit. "Regulation of programmed cell death in the developing thalamus". Thesis, University of Edinburgh, 2000. http://hdl.handle.net/1842/24709.
Testo completoHelmersson, 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.
Testo completoThomas, Marshall Peter. "Novel Roles for Ribonucleic Acids in Programmed Cell Death". Thesis, Harvard University, 2014. http://nrs.harvard.edu/urn-3:HUL.InstRepos:13094353.
Testo completoChang, 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.
Testo completoAgapite, Julie 1968. "Genetic analysis of programmed cell death in Drosophila melanogaster". Thesis, Massachusetts Institute of Technology, 2002. http://hdl.handle.net/1721.1/8321.
Testo completoIncludes 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.
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.
Testo completoRUNYAN, 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.
Testo completoKing, 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.
Testo completoYoung, 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.
Testo completoRoche, 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.
Testo completoMonetti, 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.
Testo completoThe 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
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.
Testo completoAnwar, 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.
Testo completoJohnsen, 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.
Testo completoThis 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.
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.
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.
Testo completoBlaschke-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.
Testo completoTan, 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.
Testo completoBrand, Verena Beatrice. "Programmed cell death in Plasmodium infected normal and sickle trait red blood cells". [S.l. : s.n.], 2007.
Cerca il testo completoWinbush, 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.
Testo completoWinbush, 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.
Testo completoProgrammed 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
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.
Testo completoMolostvov, 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.
Testo completoJames, 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.
Testo completoZeng, 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.
Testo completoHarvey, 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.
Testo completoNandy, Anubhab. "The Role of NFκB Factor Relish in Developmentally Programmed Cell Death". eScholarship@UMMS, 2018. https://escholarship.umassmed.edu/gsbs_diss/956.
Testo completoSobhani, 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.
Testo completoGalvin, 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.
Testo completoIncludes 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.
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.
Testo completoPh.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
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/.
Testo completoOrchard, 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/.
Testo completoZheng, 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.
Testo completoCalver, 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.
Testo completoMetzstein, 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.
Testo completoIncludes 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.
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.
Testo completoCataloged 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.
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.
Testo completoHuang, 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.
Testo completoJones, 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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