Дисертації з теми "Lipide de signalisation"
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Vaillancourt, Myriam. "Implication de la lipide phosphatase SHIP1 dans les voies de signalisation du CD32A dans le neutrophile humain." Thesis, Université Laval, 2005. http://www.theses.ulaval.ca/2005/22931/22931.pdf.
Повний текст джерелаMeuillet, Emmanuelle. "Effets des lipides membranaires sur la signalisation par les recepteurs aux facteurs de croissance : application a l'etude du mode d'action de la metformine." Strasbourg 1, 1995. http://www.theses.fr/1995STR15119.
Повний текст джерелаParadis, Sophie. "Implication du diacyglycérol pyrophosphate et des lipides phosphate phosphatases dans la signalisation de l'acide abscissique chez Arabidopsis thaliana." Paris 6, 2009. http://www.theses.fr/2009PA066531.
Повний текст джерелаWolf, Alexander. "A molecular toolbox to study the pleiotropic functions of phosphatidic acid in neurosecretion." Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ033.
Повний текст джерелаNeurosecretion requires multiple proteins acting together to orchestrate transport, fusion and recycling of secretory vesicles. However, contribution of lipids, main components of cellular membranes, have been much less studied in these processes, primarily because of a lack of adequate tools. Hence, during my thesis, I implemented two novel approaches to study the pleiotropic functions of a peculiar signaling lipid: phosphatidic acid (PA). The use of chemically modified PA click-analogues enabled me to establish their dynamics as well as to characterize their interactome directly within neurosecretory cells. A second approach based on the optogenetic targeting of enzymes involved in the PA metabolism modulated its cellular levels with an unprecedented spatial and temporal resolution. This work allowed to unravel the non-redundant functions of various subcellular PA pools. Our novel molecular toolbox for PA, represents a breakthrough in lipid biology that will greatly improve our understanding of the roles of PA in the neurosecretory process
Violet, Pierre-Christian. "Rôle des lipides-phosphate phosphatases dans la modulation des voies de signalisation impliquées dans les léiomyomes utérins." Phd thesis, Université Paris Sud - Paris XI, 2012. http://tel.archives-ouvertes.fr/tel-00788479.
Повний текст джерелаDesbourdes, Céline. "Nucléoside diphosphate kinase D : une protéine mitochondriale bifonctionnelle." Thesis, Université Grenoble Alpes (ComUE), 2017. http://www.theses.fr/2017GREAV004/document.
Повний текст джерелаThe nucleoside diphosphate kinases (NDPK) are essential for generation of nucleoside triphosphates (NTPs) using ATP and NDPs. The mitochondrial NDPK isoform (NDPK-D) located in the mitochondrial intermembrane space is found to have two modes of function. First, the phosphotransfer mode in which the protein has a kinase activity like other NDPK enzymes. In this mode, NDPK-D produces GTP for the optic atrophy 1 protein (OPA1), a GTPase involved in mitochondrial fusion, and ADP for the adenylate translocator (ANT) and the mitochondrial ATPase for ATP regeneration. The second mode of function is called lipid transfer and is related to the capacity of NDPK-D to bind anionic phospholipids, especially cardiolipin (CL). In this mode, the protein can cross-link the two mitochondrial membranes and transfer CL from the inner to the outer mitochondrial membrane, which can serve as a signal for mitophagy and apoptosis. This work aims to study these NDPK-D functions in more detail. With the use of HeLa cells stably expressing the wild-type, kinase inactive (H151N mutation) or lipid binding deficient (R90D mutation) NDPK-D and mouse lung epithelial cells, we show (i) the close proximity between NDPK-D and OPA1 that leads to GTP channeling from NDPK-D to OPA1, (ii) the essential role of NDPK-D for CL externalization to the mitochondrial surface during mitophagy, serving as a recognition signal for LC3-II-autophagosomes to eliminate damaged mitochondria, (iii) the possible inhibition of CL externalization due to the presence of NDPK-D/OPA1 complexes, and (iv) a pro-metastatic phenotype of HeLa cells expressing either of the NDPK-D mutants (H151N or R90D), characterized by high invasive and migratory potential, altered proteomic profile and changed mitochondrial network structure and function. Finally, a first bacterial expression and purification strategy for full-length OPA1 has been established for future in vitro studies of NDPK-D/OPA1 complexes
Harchouni, Seddik. "Manipulation des voies de signalisation de l'énergie pour améliorer la production des biocarburants chez les organismes photosynthétiques." Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0498.
Повний текст джерелаTriacylglycerol (TAG) is a highly energetic metabolite that can be easily converted into biodiesel. TAG can be produced from both plants and microalgae. However, plants have low TAG yields in their dominant vegetative tissues. Microalgae can accumulate high amounts of TAG, but only under stress, leading to growth inhibition and limiting yield. The study and manipulation of stress and energy signaling pathways can offer new strategies to improve biomass and TAG accumulation without compromising growth. In this thesis, I studied the role of two major energy signaling pathways: the guanosine penta(tetra) phosphate (ppGpp) pathway in the chloroplast and the target of rapamycin (TOR) pathway in the cytosol. I chose to work on the moss Physcomitrella patens which is an interesting model of photosynthetic eukaryote because of its evolutionary position between algae and vascular plants. To study the role of ppGpp we created transgenic lines that inducibly express a ppGpp synthase and over-accumulate ppGpp. I found that ppGpp accumulation causes a strong inhibition of photosynthetic capacity due to the inhibition of the expression of key chloroplast encoded proteins, and also reorganization of the thylakoid membrane system into super grana. For the TOR pathway, we treated P. patens protonema with active site TOR inhibitors and showed that this cause growth inhibition in a dose dependent manner and is accompanied by TAG accumulation. The use of lipid dyes reveals a shift from small growth associated vesicles to a larger oil body structures after treatment. Further studies will allow the development of new strategies for improving biofuel production in photosynthetic organisms
Grosjean, Kevin. "Microdomaines ordonnés de la membrane plasmique végétale : caractérisation et rôle dans la signalisation associée à la défense." Thesis, Dijon, 2015. http://www.theses.fr/2015DIJOS089/document.
Повний текст джерелаRecent studies have shown the existence of lateral sub-compartmentalization of plant plasmamembrane similar to that of animal cells and yeasts. The aim of this thesis was to provide newelements to characterize this compartmentalization (physical properties of specific domains,mechanisms of their formation, determination of their size, etc...) and to study its role in thephysiology of plant cells.The development spectral confocal microscopy coupled with the use of an environment-sensitiveprobe enabled to obtain the first description at the submicron scale of plasma membrane organizationinto domains exhibiting various physical properties. These domains coexist at the plasma membranesurface of tobacco suspension cells as well as the membrane of vesicles composed of models lipids orcell plasma membrane lipids, purified plasma membrane vesicles, and protoplasts. However,differences in the lateral organization observed in these membranes have shown the importance ofphytosterols which are, through specific interactions with neighboring plant lipids such as GIPCs,essential for local formation of ordered domains. The huge diversity of plant lipids drives thecompartmentalization of the plasma membrane allowing the dynamic segregation of membranecomponents. Sterols greatly increase membrane order, whereas proteins tends to decrease it.Cytoskeleton and cell wall do alter neither presence nor organization of ordered domains of the plasmamembrane. We have also shown that the organization of these domains is transiently modified duringthe early stages of defense signaling cascade. In fact, we have identified changes in overall physicalproperties and fine lateral organization of the membrane caused by various elicitors of defensereactions, including cryptogein, a protein secreted by the oomycete Phytophthora cryptogea. We haveshown that these changes are a generic element of defense signaling cascade and depend onphosphorylation processes; oxidative burst being also a major actor of the control of the increase ofmembrane order observed during the very early stages of the signalling process. Cryptogein, whichexhibits the particular ability to trap sterols, also showed a specific capacity to increase membranefluidity and amplify the intensity of the signalling cascade, as measured by the production of reactiveoxygen species.These results open new perspectives in the understanding of cell-elicitin interactions and provide anew view on the central role of sterol composition in the lateral organization of plant plasmamembrane. They also identify membrane dynamics as a new player in the signalling cascade occurringduring plant defense
Dramane, Gado. "Etude de la signalisation calcique dans les cellules gustatives lipidiques chez la souris." Thesis, Dijon, 2012. http://www.theses.fr/2012DIJOS035/document.
Повний текст джерелаThe lipid-binding glycoprotein CD36, expressed by circumvallate papillae (CVP) of the mouse tongue, has been shown to be implicated in oro-gustatory perception of dietary lipids. We demonstrate that linoleic acid (LA) by activating sPLA2, cPLA2 and iPLA2 via CD36, produced arachidonic acid (AA) and lyso-phosphatidylcholine (Lyso-PC) which triggered Ca2+ influx in CD36-positive taste bud cells (TBC), purified from mouse CVP. LA induced the production of Ca2+ influx factor (CIF). CIF, AA and Lyso-PC exerted different actions on the opening of store-operated Ca2+ (SOC) channels, constituted of Orai proteins and regulated by STIM1, a sensor of Ca2+ depletion in the endoplasmic reticulum. We used siRNA technology and transgenic mice models and observed that CIF and Lyso-PC opened Orai1 channels whereas AA-opened Ca2+ channels were composed of Orai1/Orai3. STIM1 was found to regulate LA-induced CIF production and opening of both kinds of Ca2+ channels. Furthermore, Stim1–/– mice lost the spontaneous preference for fat, observed in wild-type animals. The CD36-positive TBC from Stim1–/– mice also failed to release serotonin into extracellular environment. Our results suggest that fatty acid-induced Ca2+ signaling, regulated by STIM1 via CD36, might be implicated in oro-gustatory perception of dietary lipids and the spontaneous preference for fat
Platre, Matthieu. "Localisation et fonction des lipides anioniques dans l'organisation cellulaire et le développement des plantes." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSEN098.
Повний текст джерелаThe « electrostatic territory» is part of the eukaryotic membrane organization and is defined by the enrichment of negatively charged phospholipids at the membrane cytosolic face. This feature is involved in the membrane recruitment of cytosolic proteins, which contain positively charged motifs and/or domains. In this work, we used Arabidopsis thaliana as a model and explored the existence of an electrostatic territory in plant cells. We found that the plasma membrane is the most anionic intracellular membrane (Simon, Platre et al., 2016 Nature Plants). This electrostatic field is maintained by lipid cooperation between, phosphatidic acid, phosphatidylserine and phosphatidylinositol-4-phosphate. The cell surface unique feature is involved in the regulation of hormonal signalling such as auxin and brassinosteroids pathways. We found that phosphatidylserine tunes the spatiotemporal dynamics of small GTPases from the Rho family. During auxin response, PS is required to cluster Rho into specialized membrane domains. We show that nanocluster formation is required for Rho-mediated auxin signaling including the regulation of endocytosis, cytoskeleton organization, morphogenesis and the root gravitropic response
Florent-Béchard, Sabrina. "Lipides et maladie d'Alzheimer : influence du statut et de la signalisation lipidiques sur la neurodégénérescence induite par le peptide AB soluble." Thesis, Vandoeuvre-les-Nancy, INPL, 2006. http://www.theses.fr/2006INPL063N/document.
Повний текст джерелаAlzheimer’s disease (AD) is a progressive dementia characterised in the early stages by synaptic loss and neurodegeneration. Currently, no effective treatments are available and the molecular mechanisms implicated are still unknown. Recent studies, including ours, indicate that the direct interaction between soluble amyloid-ß (Aß) oligomers and the plasma membrane initiates a cellular stress involving apoptotic cascades. The present work focuses on the impact of lipid status on neuronal susceptibility to the toxicity of soluble Aß peptide and on the pro-apoptotic signalling pathways. We showed that this peptide induces membrane remodelling, thereby activating pro-apoptotic pathways and inhibiting survival signalling, which leads to neuronal cell death. This was however prevented in neurons cultured in a medium supplemented with docosahexaenoic acid (DHA), an ?3 polyunsaturated fatty acid. This protective effect seems to rely on subtle local membrane remodelling due to DHA incorporation, which maintains active survival and growth pathways. DHA did not prevent either cytosolic phospholipase A2 (cPLA2) or oxidative stress upon soluble Aß peptide exposure. These two events have already been reported by our team to be implicated in a pro-apoptotic cascade leading to ceramide production due to the activation of sphingomyelinases. These enzymes very likely play a central role in Aß peptide toxicity, as pretreatments with DHA or sphingosine-1-phosphate, a well-known anti-apoptotic compound, lead to neuronal protection through the inhibition of acid sphingomyelinase. This PhD thesis demonstrates that lipids, as structural molecules as well as signalling mediators, are essential players that could be used to develop strategies for the prevention or treatment of AD
Schindler, Lamarque Mathilde. "Dérégulation de la signalisation non génomique du récepteur aux androgènes dans un modèle SBMA in vitro." Thesis, Montpellier 2, 2010. http://www.theses.fr/2010MON20177/document.
Повний текст джерелаSpinal Bulbar Muscular Atrophy (SBMA) is a progressive inherited motoneuron disease caused by the expansion of a trinucleotide (CAG) repeat in the gene coding for the androgen receptor (AR) located on the X chromosome. This rare disease causes muscle weaknesses, hypotonia, hyporeflexia, fasciculations of facial muscles in male patients. The androgen-dependent formation of cytoplasmic aggregates and nuclear inclusions are pathological hallmarks of this polyglutamine disease but their potential neurotoxicity is still under debate. We developed a SBMA model based on a doxycycline-inducible AR51Q expression system in the NSC34 hybrid cell line. We have shown that the expression of the mutated AR leads to a reduced viability and to an alteration of neurite outgrowth compared to cells expressing the normal AR20Q. The AR belongs to the nuclear receptor superfamily of transcription factors. However, recent data have put in evidence a membrane localization of AR initiating non-genomic signaling pathways. Because we have not observed insoluble aggregates, reduced viability and neurite outgrowth could not be correlated to AR aggregation. We hypothesized that motoneuron death is not only due to aggregate formation but also to the alteration of AR signaling pathways. We focused on a correlation between the AR localization in lipid rafts and the observed phenotypes. Our results highlight the deregulation of PI3K/Akt and JNK/c-jun signaling pathways induced by the expression of AR51Q in our SBMA model
Gueguinou, Maxime. "Complexe canalaires KCa/Ca sensibles aux éther-lipides : régulation de la signalisation calcique dans la migration de cellules cancéreuses." Thesis, Tours, 2015. http://www.theses.fr/2015TOUR4032.
Повний текст джерелаIn most cases of cancer, metastasis and not the primary tumor per se is the main cause of mortality. To establish secondary growth in distant organs cancer cells must develop an enhanced propensity to migrate. The key objective of this thesis proposes that some actors of Ca2+ signaling (Orai, and TRPC, STIM) coupled to SK3 channel would form complexes that play a critical role in cell migration of various cancers (breast, colon and prostate). Furthermore we showed that the localization of these channels complexes in lipid-rafts is essential to their regulation and function. Thus, the delocalization of these complexes of lipid-raft outside by alkyl-phospholipids could be a new way to modulate the SK3/Ca2+ dependent cell migration and metastasis development
Florent-Béchard, Sabrina Pillot Thierry. "Lipides et maladie d'Alzheimer influence du statut et de la signalisation lipidiques sur la neurodégénérescence induite par le peptide AB soluble /." Vandoeuvre-les-Nancy : INPL, 2006. http://www.scd.inpl-nancy.fr/theses/2006_FLORENT_BECHARD_S.pdf.
Повний текст джерелаPierrugues, Olivier (19. "Caractérisation moléculaire de deux gènes AtPap2, codant des lipides phosphate phosphatases chez Arabidopsis : implication potentielle d'AtPap2a dans la signalisation du stress." Aix-Marseille 1, 2000. http://www.theses.fr/2000AIX11021.
Повний текст джерелаPendaries, Caroline. "Synthèse et rôle d'un nouveau second messager lipidique : le phosphatidylinositol 5-phosphate." Toulouse 3, 2005. http://www.theses.fr/2005TOU30141.
Повний текст джерелаBesides their structural role as membrane components, phospholipids play an active part in the regulation of many intracellular signalling pathways. This is particularly the case for phosphoinositides that act as precursors of second messengers or that govern signaling pathways in a spatio-temporal manner. Phosphoinositides levels are tightly controled by specific kinases, phosphatases and phopholipases, and deregulation of some of these enzymes have been linked to pathologies such as cancers or genetic diseases. Recently, a new phosphoinositide, the phosphatidylinositol 5-phosphate (PI(5)P), has been identified. We have studied the function of PI(5)P using an infection model with the pathogen Shigella flexneri. During invasion, the bacteria injects in the host cell the PI(4,5)P2 4-phosphatase, IpgD, that was shown to convert most of the PI(4,5)P2 into PI(5)P. This conversion induces the activation of the Akt oncogenic pathway. Specific probes that bind PI(5)P enable us to colocalize this lipid with activated Akt at entry foci. .
Tellier, Edwige. "Le TNF alpha : maturation par ADAM-17 et activation d'une voie de signalisation sphingomyéline-céramide." Toulouse 3, 2008. http://thesesups.ups-tlse.fr/725/.
Повний текст джерелаTNF alpha (Tumor Necrosis Factor alpha) is a pro-inflammatory cytokine existing in two molecular forms, a transmembrane form cleaved to produced a soluble form. TNF alpha is implicated in numerous physiological and physiopathologicals processes such as atherosclerosis. Within the lesions, soluble TNF alpha seems to play a major role : genetically modified mice expressing exclusively a transmembrane form of TNF alpha develop atherosclerosis lesions with an inflammatory state which is significantly reduced compared to lesions of wild type mice (Canault et al. , 2004). Cleavage of TNF alpha transmembrane form is due to the metalloproteinase ADAM-17 (A Disintegrine and Metalloproteinase-17). Today, regulation of ADAM-17 cleavage activity is poorly documented. We have voiced hypothesis that the membrane localization of ADAM-17 and its substrates was implicated to its regulation. We show that ADAM-17 mature form is localized into membrane particular domains, the lipid rafts (Tellier et al. , 2006) and that this localization determined its activity. We also show that cell cholesterol homeostasis modifications by HDLs lead to a ADAM-17 substrates cleavage perturbations (Tellier et al. , 2007). TNF alpha induce number signaling pathways in atherosclerosis plaques cells, leading to several effects including SMC (smooth muscle cells) proliferation. Literature show that TNF alpha active neutral sphingomyelinase (nSMase) and that nSMase mitogene effect involve MMP2 and MT1-MMP (Auge et al. , 2004 ; Nègre-Salvayre et al. , 2005). We have postulated that TNF alpha could induce cell proliferation by a pathway implicating metalloproteinases and neutral SMase activation. Our results show that TNF alpha induced mesenchymal cells proliferation is due to pro-protein convertase furin, MT1-MMP ad MMP2 metalloproteinases sequential activation followed by sphingomyeline/ceramide pathway (Tellier et al. , 2008). In conclusion, our results give new data on the TNF alpha biodisponibility regulation as on pro-atherogene effect via stress mitogene pathway activation
Fradagrada, Alexandre. "Exploration moléculaire de nouvelles voies d'endocytose et de trafic intracellulaire : Rôle dans la signalisation de l'interféron gamma et le transport des lipides." Paris 11, 2005. http://www.theses.fr/2005PA11T026.
Повний текст джерелаFaure, Lionel. "Identification et caractérisation de la première N-acylphosphatidyléthanolamine synthase chez Arabidopsis thaliana." Thesis, Bordeaux 2, 2009. http://www.theses.fr/2009BOR21630/document.
Повний текст джерелаDiscovery and characterization of an A. thaliana N-acylphosphatidylethanolamine synthase. N-acylphosphatidylethanolamine (NAPE) is a widespread, albeit minor, membrane phospholipid in various organisms. Besides its stabilizing properties to membranes bilayers, NAPE is known to be the precursor for N-acylethanolamine (NAE) synthesis. NAE have been shown to regulate a variety of physiological functions in both plants (germination, root development, gene induction, etc.) and animals (apoptosis, ligand for cannabinoid receptors, satiety properties, etc.) At the beginning of my PhD, the genes encoding the enzymes involved in the different steps of NAE metabolism were well characterized (e.g NAPE-PLD, FAAH 1 and 2), with the exception of the NAPE synthase gene(s). A bioinformatic study allowed the identification of coding sequences for putative new acyltransferases in A. thaliana, such as the At1g78690 gene. After expression in E. coli, the functional characterization of At1g78690p was carried out by analyses of the lipid content and by enzymatic assays using membrane fractions or purified proteins. The localisation of the protein and its activity were also studied in A. thaliana mutants (ADN-T and “35S”). This study shows the identification and characterization of the first NAPE-synthase in plants
Abdoul-Azize, Souleymane. "Implication de la signalisation calcique et des MAP kinases dans la perception gustative lipidique." Phd thesis, Université de Bourgogne, 2013. http://tel.archives-ouvertes.fr/tel-01018378.
Повний текст джерелаKalachova, Tetiana. "Role de la signalisation lipidique chez les plantes en réponse aux contraintes de l'environnement et lors du développement." Thesis, Paris Est, 2017. http://www.theses.fr/2017PESC1114/document.
Повний текст джерелаThesis is devoted to the investigation of lipid signaling processes as a universal mechanism mediating cellular responses to phytohormones and elicitors thus playing a key role in cell metabolism remodeling during plant adaptation to environmental changes. Phospholipase D (PLD) and its product phosphatidic acid (PA) were found to be involved to the SA-induced signaling cascades in Arabidopsis thaliana guard cells. Using radioactive labeling of phospholipids we found an activation of PLD and production of PA in leaves of 4-week old plants after salicylic acid (SA) treatment. Using histochemical assay, inhibitor assay and transgenic lines knock-out by different isoforms of NADPH-oxidases, we showed the involvement of PLD and NADPH-oxidase RbohD to PA-mediated superoxide formation in Arabidopsis tissues infiltrated by SA and SA-induced stomatal closure. SA- crosstalk with abscisic acid (ABA) in transcriptome remodeling induced by these hormones was investigated in suspension cell culture. Both SA and ABA inhibited basal activity of phosphatidylinositol dependent phospholipase C (PI-PLC) in vivo, while SA (but not ABA) also induced the phosphorylation of phosphatidylinositols. Total transcriptomes of suspension cells after SA or ABA treatment were compared to those obtained from suspension cells treated with U73122 (PI-PLC inhibitor) or wortmannin (inhibitor of phosphatidylinositol-4-kinases (PI4K) that provide the substrate for PI-PLC catalyzed reactions). We found a specific gene clusters, for those the effect of ABA and inhibitors was similar; SA-dependent genes, regulated via the balance of phosphoinositides, and SA-dependent genes, regulated via PLD-mediated pathway. Based on the bioinformatic analysis of the promoters of all selected gene sets, we claim a phosphoinositides level regulation to be an important factor mediating basal cell transcriptome and expression changes induced by SA and ABA.The effect of bacterial peptide flg22 on phospholipid turnover was detected in both suspension cells and seedlings. Flg22 induced accumulation of PA by the activation of PI-PLC coupled with diacylglycerolkinase (DGK) and a corresponding parallel increase of phosphatidylinositol-4,5-biphosphate content, that is a substrate of PI-PLC. Inhibitor analysis revealed the involvement of Ca2+ ions in lipid signaling enzymes reaction to flagellin treatment. We showed the role of DGK and PI-PLC in production of reactive oxygen species (ROS) induced by flg22. PA-production was placed in signaling cascade downstream of flagellin recognition by FLS2-BAK1 receptor complex receptor, but upstream or ROS formation by NADPH-oxidase RbohD. DGK5 was found to be the main source of the detected PA. The role of DGK5 was characterized in basal transcriptome regulation and its flagellin-induced remodeling; in flg22-induced callose accumulation in apoplast and resistance to biotrophic pathogen Pseudomonas syringae pv tomato DC3000. We proposed a new model of flagellin perception that includes PI-PLC and DGK5. Role of phosphoinositides in auxin and cytokinin signaling cascades was revealed studying root morphogenesis in Arabidopsis mutant pi4kb1b2 deficient for two PI4K genes, and pi4kb1b2sid2 that had additional mutation it key enzyme of SA biosynthesis, thus allowing us to separate SA-dependent and independent effects of the PI4K deficiency. pi4kb1b2 mutant plants exhibit the dwarf phenotype both in leaf and root parts, while pi4kb1b2sid2 show the normal rosette growth compared to WT, but still shorter roots. We analyzed root meristem anatomy, cortical cells elongation, gravitropic response, responses to exogenic hormones and firstly showed the connection of PI4K activity with auxin and cytokinin effects during root morphogenesis and gravitropism. Our results broaden the knowledge about the nature of plant phytohormonal signaling and can be used as a basis for increasing the resistance of agriculturally important crop plants to environmental stresses
Ferlin, Juliette. "Etude de la voie de signalisation GBF1-ARF au cours de la réplication virale." Thesis, Lille 2, 2018. http://www.theses.fr/2018LIL2S047.
Повний текст джерелаGBF1 has recently emerged as a cellular factor essential for the replication of single-stranded positive-sense RNA ((+)RNA) viruses from different families. GBF1 is a guanine-nucleotide exchange factor of small G proteins of the Arf family, known to regulate the early secretory pathway. By studying the hepatitis C virus (HCV) as a model, we have shown that the role of GBF1 in viral replication is distinct from its regulatoryfunction of the sercretory pathway. Indeed, GBF1 function in HCV replication is mediated by Arf4 and Arf5,whereas another pair, Arf1 and Arf4, mediates the regulation of the secretion. To determine if this mechanism ofaction is conserved among (+)RNA viruses, we showed that GBF1 is involved in yellow fever virus (YFV),sindbis virus (SINV), human coronavirus 229E (HCoV-229E) and coxsackievirus B4 (CVB4) infection. Our results indicate that YFV, SINV and HCoV-229E infections are Arf4 and Arf5 dependent, as we previouslyshowed for HCV. However, YFV and SINV would also use another Arf pair, Arf1 and Arf4, during their lifecycle. In addition, CVB4 infection depends on GBF1, but doesn’t seem to depend on any Arf. Although GBF1 is required for (+)RNA viruses replication, its mechanism of action appears not to be conserved.The Arf4-Arf5 pair appears to be involved in the replication of several (+)RNA viruses. However, these twoproteins have been poorly studied so far, contrary to Arf1. Our hypothesis is that the Arf4-Arf5 pair regulatesspecific effectors involved in viral replication. Our results indicate that Arf4 and Arf5 simultaneous depletionalters the morphology of the Golgi apparatus, which becomes condense, and of lipid droplets (LD), whichaccumulate and grow bigger at the cell periphery. However, a lipidomic analysis of Arf4 and Arf5 depleted cellsdisplayed an unaltered lipid composition, which suggests a morphologic impact on LD, rather than a disruptionof the lipid metabolism. A transcriptomic analysis identified proteins up- or down-regulated after Arf4 and Arf5 depletion. We assessed the function of some of these proteins in HCV replication, but none of them proved implicated.In conclusion, our results hightlighed new GBF1 functions, mediated by the pair Arf4-Arf5. Arf4 and Arf5 are involved in regulating the morphology of Golgi complex and of LDs, as well as the replication of (+) RNA viruses. It remains to assess if these functions are independent or related to each other, and which specific effectors they use
Noack, Lise. "Rôle du complexe AtPI4Kalpha1 dans l’établissement de l’identité de la membrane plasmique et le développement chez Arabidopsis thaliana." Thesis, Lyon, 2020. http://www.theses.fr/2020LYSEN066.
Повний текст джерелаEukaryotic cells are composed of several membrane-surrounded compartments. Each compartment has a unique physicochemical environment delimited by a membrane with a specific biochemical and biophysical identity. The membrane identity includes the nature of the lipids, the curvature, the electrostaticity and the density of lipids at the membrane. The identity of each membrane allows the proper localization of membrane-associated proteins. Phosphoinositides are rare anionic lipids present in membranes. Five types of phosphoinositides exist in plants - PI3P, PI4P, PI5P, PI(4,5)P2 and PI(3,5)P2 - depending of the number and the position of phosphates around the inositol ring. They accumulate differently at the plasma membrane and in intracellular compartments and interact with proteins through stereo-specific or electrostatic interactions. Recent work uncovered that PI4P concentrates according to an inverted gradient by comparison to their yeast and animal counterpart. In plants, PI4P massively accumulates at the plasma membrane and is present in fewer amounts at the trans-Golgi Network (TGN). This PI4P accumulation at the cell surface drives the plasma membrane electrostatic field, which in turn recruits a host of signalling proteins to this compartment. Moreover the plant TGN is the place of vesicular secretion but is also involved in endocytic sorting and recycling, which might imply regulatory mechanisms of lipid exchanges or membrane identity maintenance between the plasma membrane and the TGN. Here, we characterized PI4Kα1 mutants and showed that pi4kα1 loss-of-function leads to pollen grain lethality and distortion in the allele transmission via the female gametophyte, while its knockdown displayed strong developmental phenotypes. Using yeast two hybrid screening and mass spectrometry, we identified that PI4Kα1 is part of an heterotetrameric complex composed of NO POLLEN GERMINATION (NPG), EFR3 OF PLANTS (EFOP) and HYCCIN (HYC). The interaction between PI4Kα1 and the structural subunits of the complex is essential to target PI4Kα1 at the plasma membrane. In addition, we showed that PI4Kα1 complex is anchored in immobile and predefined subdomains of the plasma membrane. This work opens new perspectives on the role of the PI4Kα1 complex in plasma membrane suborganization
Kress, Alla. "Probing molecular orientational order of lipid reporters and MHC Class I protein in cell membranes using polarization-resolved fluorescence imaging." Thesis, Aix-Marseille 3, 2011. http://www.theses.fr/2011AIX30046.
Повний текст джерелаBiomolecular orientational organization of lipids and proteins in the plasma membrane is a crucial factor in biological processes where functions can be closely related to orientation and ordering mechanisms. The concept of transient nanosized phase separations in ordered and disordered domains, called "lipid rafts" is now widely accepted. Furthermore, the ordered domains are enriched in signaling proteins, which highlights the crucial impact of phase separation during the signaling processes. While this field has been so far largely addressed by studying the translational diffusion behavior of membrane proteins and lipid reporters by Single Molecule Tracking (SMT) or Fluorescence Correlation Spectroscopy (FCS), only little is known about the orientational behavior of signaling proteins and lipid reporters in the plasma membrane. In this PhD thesis we investigated the molecular orientational order of the signaling molecule MHC Class I protein using fluorescence anisotropy imaging as well as of lipid reporter di-8-ANEPPQ using polarization-resolved fluorescence imaging. Fluorescence anisotropy imaging requires a fluorescent label rigidly attached to the system under study, able to report its orientational order behavior. Thus, MHC Class I protein has been successfully labeled in a rigid way. We analyzed the orientational order of MHC Class I protein quantitatively in the endomembrane and plasma membrane and we found that the orientational order of MHC Class I protein in both membranes depends primarily on the maturation state of the protein and its interaction with the cytoskeleton
Laulagnier, Karine. "Caractérisation lipidique des exosomes de mastocytes et de cellules dendritiques : rôle de la phospholipase D2 dans leur biogénèse." Toulouse 3, 2004. http://www.theses.fr/2004TOU30073.
Повний текст джерелаExosomes are small vesicles (60-90nm) secreted by different immune cells and which are able to induce anti-tumoral immunity. During this PhD, we have shown that exosomes from mast cells displayed a special lipid composition. Their membranes are particularly rigid and display a high flip-flop speed. Then, inactivation of phospholipase D2 (PLD2), an enzyme producing a fusogenic lipid, phosphatidic acid, decreases exosomes secretion. Moreover, PLD2 is enriched and active on exosomes and could be involved in interaction mechanisms between exosomes and their target cells. Finally, we have shown that this interaction led to internalisation of exosomes by their target cells. Thus, this PhD allowed to establish lipid structure of exosomes and to better understand their biogenesis and their interaction with target cells. Later, these results could contribute to promote anti-tumoral therapies using exosomes
Yu, Lingli. "Nerve Growth Factor Signaling from Membrane Microdomain to Nucleus : Differential Regulation by Caveolins." Phd thesis, Ecole normale supérieure de lyon - ENS LYON, 2012. http://tel.archives-ouvertes.fr/tel-00796393.
Повний текст джерелаBertazzi, Dimitri. "Analyse des mécanismes cellulaires responsables de maladies neurodégénératives dans le modèle de la levure Saccharomyces cerevisiae : analyse fonctionnelle de myotubularines responsables de pathologies humaines." Phd thesis, Université de Strasbourg, 2012. http://tel.archives-ouvertes.fr/tel-01070634.
Повний текст джерелаBassot, Arthur. "Rôle des points de contact Réticulum Endoplasmique-Mitochondrie (MAMs) dans la régulation du métabolisme glucido-lipidique du foie et importance du Monoxyde d’Azote (NO)." Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1290.
Повний текст джерелаThe endoplasmic reticulum and mitochondria are two major organelles involved in the regulation of glucose and lipid metabolism. These structures interact at close contact points called Mitochondria-Associated Endoplasmic Reticulum Membranes (MAMs). MAMs constitute an area of communication and exchange, of lipids and calcium among others, essential for the activity of both organelles and the maintenance of cellular homeostasis. Physical connections are ensured by the interaction of complementary proteins, such as the voltage-dependent anionic channel (VDAC)-1, the chaperone protein (Grp)-75 and the inositol 1,4,5-triphosphate receptor (IP3R)-1, constituting a complex involved in calcium transfer. Other actors such as mitofusins 1 and 2 (MFN1/2) also connect the two organelles and are involved in lipid exchanges. Recently, MAMs have emerged as a new carrefour for insulin signaling in the liver. Nitric oxide (NO) also helps control the response to hepatic insulin and has a specific action on mitochondria. My thesis work showed that NO at physiological concentrations modulates the interactions between RE and mitochondria in the liver and that its action on MAMs involves the sGC/cGMP/PKG signalling pathway. I also demonstrated that NO modulation of MAMs plays a key role in regulating the insulin signaling pathway (project 1). In addition, I explored the importance of MAMs in the regulation of lipid metabolism. For that purpose, protein expression of Grp75 and Mfn2 was modulated in a human hepatocarcinoma model (Huh7). Results showed that overexpression of both proteins improves MAMs and mitochondrial β-oxidation but leads to intracellular lipid accumulation. This could be due to a defect in lipid secretion in VLDL lipoproteins and could imply the appearance of mitochondrial stress and an alteration of phospholipid exchanges between the two organelles (project 2). Consequently, my work confirms the physiological role of MAMs and sheds light on the mechanisms of action of this cellular platform in the regulation of glucose and lipid metabolism in the liver. In the longer term, this knowledge may contribute to the identification of potential therapeutic targets to prevent steatosis and hepatic insulin resistance and their complications
Gonon, Géraldine. "Space radiation-induced bystander effect : kinetics of biologic responses, mechanisms, and significance of secondary radiations." Phd thesis, Université de Franche-Comté, 2011. http://tel.archives-ouvertes.fr/tel-00987717.
Повний текст джерела"Implication de la lipide phosphatase SHIP1 dans les voies de signalisation du CD32A dans le neutrophile humain." Thesis, Université Laval, 2005. http://www.theses.ulaval.ca/2005/22931/22931.pdf.
Повний текст джерелаDodelet-Devillers, Aurore. "The importance of the Hedgehog signaling pathway at the level of the blood-brain barrier." Thèse, 2009. http://hdl.handle.net/1866/3631.
Повний текст джерелаThe blood-brain barrier (BBB), composed of tightly bound endothelial cells (ECs), regulates the entry of blood-borne molecules and immune cells into the CNS. Recent studies indicate that the Hedgehog (Hh) signaling pathway in adult tissues plays an important role in vascular proliferation, differentiation and tissue repair. Using a lipid membrane raft-based proteomic approach, I have identified the Hedgehog (Hh) pathway as a signaling cascade involved in preserving and upkeeping BBB functions. My study shows that human astrocytes express and secrete Sonic Hh (Shh) and conversely, that human BBB-ECs bear the Hh receptor Patched-1 (Ptch-1), the signal transducer Smoothened (Smo) as well as transcription factors of the Gli family. Furthermore, activation of the Hh pathway in BBB-ECs restricts the passage of soluble tracers in vitro. By blocking the Hh signaling in vitro and by using Shh knock-out (-/-) embryonic mice, I demonstrate a reduced expression of TJ molecules claudin-5, occludin and ZO-1. Hh activation also decreases the surface expression of cell adhesion molecules ICAM-1 and VCAM-1, and decreases BBB-ECs secretion of pro-inflammatory chemokines IL-8/CXCL8 and monocytes chemoattractant protein 1 MCP-1/CCL2, resulting in a reduction of migrating CD4+ lymphocytes across human BBB-EC monolayers. In vitro treatment with inflammatory cytokines TNF-α and IFN-γ, upregulates the production of astrocytic Shh and the BBB-EC surface expression of Ptch-1 and Smo. In active Multiple Sclerosis (MS) lesions, in which the BBB is disrupted, Shh expression is drastically upregulated in hypertrophic astrocytes, while Ptch-1 and Smo expression is down-regulated or left unchanged, suggesting that a deregulation in the Hh signaling pathway may prevent the barrier stabilizing properties of Hh. Our data demonstrate an anti-inflammatory and BBB-promoting effect of astrocyte-secreted Hh and suggest that a pro-inflammatory environment disrupt the BBB by impacting, at least in part, on Hh signaling in brain ECs.