Bibliografías temáticas / Lysosomes

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Literatura académica sobre el tema "Lysosomes"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 9 de junio de 2025

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Artículos de revistas sobre el tema "Lysosomes"

1

Nakae, Isei, Tomoko Fujino, Tetsuo Kobayashi, Ayaka Sasaki, Yorifumi Kikko, Masamitsu Fukuyama, Keiko Gengyo-Ando, Shohei Mitani, Kenji Kontani, and Toshiaki Katada. "The Arf-like GTPase Arl8 Mediates Delivery of Endocytosed Macromolecules to Lysosomes inCaenorhabditis elegans." Molecular Biology of the Cell 21, no. 14 (July 15, 2010): 2434–42. http://dx.doi.org/10.1091/mbc.e09-12-1010.

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Late endocytic organelles including lysosomes are highly dynamic acidic organelles. Late endosomes and lysosomes directly fuse for content mixing to form hybrid organelles, from which lysosomes are reformed. It is not fully understood how these processes are regulated and maintained. Here we show that the Caenorhabditis elegans ARL-8 GTPase is localized primarily to lysosomes and involved in late endosome-lysosome fusion in the macrophage-like coelomocytes. Loss of arl-8 results in an increase in the number of late endosomal/lysosomal compartments, which are smaller than wild type. In arl-8 mutants, late endosomal compartments containing endocytosed macromolecules fail to fuse with lysosomal compartments enriched in the aspartic protease ASP-1. Furthermore, loss of arl-8 strongly suppresses formation of enlarged late endosome-lysosome hybrid organelles caused by mutations of cup-5, which is the orthologue of human mucolipin-1. These findings suggest that ARL-8 mediates delivery of endocytosed macromolecules to lysosomes by facilitating late endosome-lysosome fusion.
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2

Trivedi, Purvi C., Jordan J. Bartlett, and Thomas Pulinilkunnil. "Lysosomal Biology and Function: Modern View of Cellular Debris Bin." Cells 9, no. 5 (May 4, 2020): 1131. http://dx.doi.org/10.3390/cells9051131.

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Lysosomes are the main proteolytic compartments of mammalian cells comprising of a battery of hydrolases. Lysosomes dispose and recycle extracellular or intracellular macromolecules by fusing with endosomes or autophagosomes through specific waste clearance processes such as chaperone-mediated autophagy or microautophagy. The proteolytic end product is transported out of lysosomes via transporters or vesicular membrane trafficking. Recent studies have demonstrated lysosomes as a signaling node which sense, adapt and respond to changes in substrate metabolism to maintain cellular function. Lysosomal dysfunction not only influence pathways mediating membrane trafficking that culminate in the lysosome but also govern metabolic and signaling processes regulating protein sorting and targeting. In this review, we describe the current knowledge of lysosome in influencing sorting and nutrient signaling. We further present a mechanistic overview of intra-lysosomal processes, along with extra-lysosomal processes, governing lysosomal fusion and fission, exocytosis, positioning and membrane contact site formation. This review compiles existing knowledge in the field of lysosomal biology by describing various lysosomal events necessary to maintain cellular homeostasis facilitating development of therapies maintaining lysosomal function.
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Amick, Joseph, Arun Kumar Tharkeshwar, Catherine Amaya,, and Shawn M. Ferguson. "WDR41 supports lysosomal response to changes in amino acid availability." Molecular Biology of the Cell 29, no. 18 (September 2018): 2213–27. http://dx.doi.org/10.1091/mbc.e17-12-0703.

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C9orf72 mutations are a major cause of amyotrophic lateral sclerosis and frontotemporal dementia. The C9orf72 protein undergoes regulated recruitment to lysosomes and has been broadly implicated in control of lysosome homeostasis. However, although evidence strongly supports an important function for C9orf72 at lysosomes, little is known about the lysosome recruitment mechanism. In this study, we identify an essential role for WDR41, a prominent C9orf72 interacting protein, in C9orf72 lysosome recruitment. Analysis of human WDR41 knockout cells revealed that WDR41 is required for localization of the protein complex containing C9orf72 and SMCR8 to lysosomes. Such lysosome localization increases in response to amino acid starvation but is not dependent on either mTORC1 inhibition or autophagy induction. Furthermore, WDR41 itself exhibits a parallel pattern of regulated association with lysosomes. This WDR41-dependent recruitment of C9orf72 to lysosomes is critical for the ability of lysosomes to support mTORC1 signaling as constitutive targeting of C9orf72 to lysosomes relieves the requirement for WDR41 in mTORC1 activation. Collectively, this study reveals an essential role for WDR41 in supporting the regulated binding of C9orf72 to lysosomes and solidifies the requirement for a larger C9orf72 containing protein complex in coordinating lysosomal responses to changes in amino acid availability.
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4

Bonet-Ponce, Luis, Alexandra Beilina, Chad D. Williamson, Eric Lindberg, Jillian H. Kluss, Sara Saez-Atienzar, Natalie Landeck, et al. "LRRK2 mediates tubulation and vesicle sorting from lysosomes." Science Advances 6, no. 46 (November 2020): eabb2454. http://dx.doi.org/10.1126/sciadv.abb2454.

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Genetic variation around the LRRK2 gene affects risk of both familial and sporadic Parkinson’s disease (PD). However, the biological functions of LRRK2 remain incompletely understood. Here, we report that LRRK2 is recruited to lysosomes after exposure of cells to the lysosome membrane–rupturing agent LLOME. Using an unbiased proteomic screen, we identified the motor adaptor protein JIP4 as an LRRK2 partner at the lysosomal membrane. LRRK2 can recruit JIP4 to lysosomes in a kinase-dependent manner via the phosphorylation of RAB35 and RAB10. Using super-resolution live-cell imaging microscopy and FIB-SEM, we demonstrate that JIP4 promotes the formation of LAMP1-negative tubules that release membranous content from lysosomes. Thus, we describe a new process orchestrated by LRRK2, which we name LYTL (LYsosomal Tubulation/sorting driven by LRRK2), by which lysosomal tubulation is used to release vesicles from lysosomes. Given the central role of the lysosome in PD, LYTL is likely to be disease relevant.
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5

Bakker, A. C., P. Webster, W. A. Jacob, and N. W. Andrews. "Homotypic fusion between aggregated lysosomes triggered by elevated [Ca2+]i in fibroblasts." Journal of Cell Science 110, no. 18 (September 15, 1997): 2227–38. http://dx.doi.org/10.1242/jcs.110.18.2227.

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Previous studies demonstrated that microinjection of antibodies to the cytoplasmic domain of the lysosomal glycoprotein lgp120 induces aggregation of lysosomes in NRK cells. Here we show that the antibody-clustered vesicles do not co-localize with MPR and ss-COP-containing organelles, confirming their lysosomal nature. Observations by transmission and high voltage electron microscopy indicated that, although tightly apposed to each other, aggregated lysosomes remained as separate vesicles, with an average diameter of 0.3-0.4 micron. However, when cells microinjected with antibody were exposed to the Ca2+ ionophore ionomycin, large vesicles were formed within the lysosome clusters, suggesting the occurrence of lysosome-lysosome fusion. Stereological measurements of lysosome diameters on confocal and transmission electron microscopy indicated that the large lgp120-positive vesicles could have originated from the fusion of 3 up to 15 individual lysosomes. To verify if agents that mobilize Ca2+ from intracellular stores had the same effect, anti-lgp120-microinjected cells were treated with thapsigargin, and with the receptor-mediated agonists bombesin and thrombin. Thapsigargin also induced the formation of large lgp120-containing vesicles, detected by both confocal and transmission electron microscopy. Analysis of antibody-clustered lysosomes in streptolysin O-permeabilized cells indicated that an intracellular free Ca2+ concentration of 1 microM was sufficient to trigger formation of large lysosomes.
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6

Xu, Miao, Ke Liu, Manju Swaroop, Wei Sun, Seameen J. Dehdashti, John C. McKew, and Wei Zheng. "A Phenotypic Compound Screening Assay for Lysosomal Storage Diseases." Journal of Biomolecular Screening 19, no. 1 (August 27, 2013): 168–75. http://dx.doi.org/10.1177/1087057113501197.

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The lysosome is a vital cellular organelle that primarily functions as a recycling center for breaking down unwanted macromolecules through a series of hydrolases. Functional deficiencies in lysosomal proteins due to genetic mutations have been found in more than 50 lysosomal storage diseases that exhibit characteristic lipid/macromolecule accumulation and enlarged lysosomes. Recently, the lysosome has emerged as a new therapeutic target for drug development for the treatment of lysosomal storage diseases. However, a suitable assay for compound screening against the diseased lysosomes is currently unavailable. We have developed a Lysotracker staining assay that measures the enlarged lysosomes in patient-derived cells using both fluorescence intensity readout and fluorescence microscopic measurement. This phenotypic assay has been tested in patient cells obtained from several lysosomal storage diseases and validated using a known compound, methyl-β-cyclodextrin, in primary fibroblast cells derived from Niemann Pick C disease patients. The results demonstrate that the Lysotracker assay can be used in compound screening for the identification of lead compounds that are capable of reducing enlarged lysosomes for drug development.
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7

Cuervo, A. M., E. Knecht, S. R. Terlecky, and J. F. Dice. "Activation of a selective pathway of lysosomal proteolysis in rat liver by prolonged starvation." American Journal of Physiology-Cell Physiology 269, no. 5 (November 1, 1995): C1200—C1208. http://dx.doi.org/10.1152/ajpcell.1995.269.5.c1200.

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Lysosomal uptake and degradation of polypeptides such as glyceraldehyde-3-phosphate dehydrogenase (GAPDH), ribonuclease A (RNase A), and RNase S-peptide (residues 1-20 of RNase A) are progressively activated in rat liver by starvation before isolation of lysosomes. This pathway of proteolysis is selective, since it is stimulated by the heat shock cognate protein of 73 kDa (HSC73) and ATP-MgCl2, and lysosomal uptake of RNase A could be competed by GAPDH but not by ovalbumin. A portion of intracellular HSC73 is associated with certain lysosomes, and the amount of lysosomal HSC73 increases by 5- to 10-fold during prolonged starvation. The lysosome-associated HSC73 is primarily within the lysosomal lumen. Double immunogold labeling of lysosomes incubated in vitro with RNase A detects this protein substrate as well as HSC73 within lysosomes. More than two-thirds of the labeled lysosomes contain both RNase A and HSC73. The possible physiological significance of the activation of this selective pathway of lysosomal proteolysis in long-term starvation is discussed.
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8

Liu, Ji, Wennan Lu, Sonia Guha, Gabriel C. Baltazar, Erin E. Coffey, Alan M. Laties, Ronald C. Rubenstein, William W. Reenstra, and Claire H. Mitchell. "Cystic fibrosis transmembrane conductance regulator contributes to reacidification of alkalinized lysosomes in RPE cells." American Journal of Physiology-Cell Physiology 303, no. 2 (July 15, 2012): C160—C169. http://dx.doi.org/10.1152/ajpcell.00278.2011.

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The role of the cystic fibrosis transmembrane conductance regulator (CFTR) in lysosomal acidification has been difficult to determine. We demonstrate here that CFTR contributes more to the reacidification of lysosomes from an elevated pH than to baseline pH maintenance. Lysosomal alkalinization is increasingly recognized as a factor in diseases of accumulation, and we previously showed that cAMP reacidified alkalinized lysosomes in retinal pigmented epithelial (RPE) cells. As the influx of anions to electrically balance proton accumulation may enhance lysosomal acidification, the contribution of the cAMP-activated anion channel CFTR to lysosomal reacidification was probed. The antagonist CFTRinh-172 had little effect on baseline levels of lysosomal pH in cultured human RPE cells but substantially reduced the reacidification of compromised lysosomes by cAMP. Likewise, CFTR activators had a bigger impact on cells whose lysosomes had been alkalinized. Knockdown of CFTR with small interfering RNA had a larger effect on alkalinized lysosomes than on baseline levels. Inhibition of CFTR in isolated lysosomes altered pH. While CFTR and Lamp1 were colocalized, treatment with cAMP did not increase targeting of CFTR to the lysosome. The inhibition of CFTR slowed lysosomal degradation of photoreceptor outer segments while activation of CFTR enhanced their clearance from compromised lysosomes. Activation of CFTR acidified RPE lysosomes from the ABCA4−/− mouse model of recessive Stargardt's disease, whose lysosomes are considerably alkalinized. In summary, CFTR contributes more to reducing lysosomal pH from alkalinized levels than to maintaining baseline pH. Treatment to activate CFTR may thus be of benefit in disorders of accumulation associated with lysosomal alkalinization.
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Alquier, C., P. Guenin, Y. Munari-Silem, C. Audebet, and B. Rousset. "Isolation of pig thyroid lysosomes. Biochemical and morphological characterization." Biochemical Journal 232, no. 2 (December 1, 1985): 529–37. http://dx.doi.org/10.1042/bj2320529.

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Open thyroid follicles were prepared by mechanical disruption of pig thyroid fragments through a metal sieve. This procedure allowed preparation of thyroid-cell material depleted of colloid thyroglobulin. Open thyroid follicles were used to prepared a crude particulate fraction, which contained lysosomes, mitochondria and endoplasmic reticulum. These organelles were subfractionated by isopycnic centrifugation on iso-osmotic Percoll gradients. A lysosomal peak was identified by its content of acid hydrolases: acid phosphatase, cathepsin D, β-galactosidase and β-glucuronidase. The lysosomal peak was well separated from mitochondria and endoplasmic reticulum. The lysosomal peak, from which Percoll was removed by centrifugation, was taken as the purified lysosome fraction (L). Lysosomes of fraction L were purified 45-55-fold (as compared with the homogenate) and contained about 5% of the total thyroid acid hydrolase activities. Electron microscopy showed that fraction L was composed of an approx. 90% pure population of lysosomes, with an average diameter of 220 nm. Acid hydrolase activities were almost completely (80-90%) released by an osmotic-pressure-dependent lysis. Thyroglobulin was identified by polyacrylamide-gel electrophoresis as a soluble component of the lysosome fraction. In conclusion, a 50-fold purification of pig thyroid lysosomes was achieved by using a new tissue-disruption procedure and isopycnic centrifugation on Percoll gradient. The presence of thyroglobulin indicates that the lysosome population is probably composed of primary and secondary lysosomes. Isolated thyroid lysosomes should serve as an interesting model to study the reactions whereby thyroid hormones are generated from thyroglobulin and released into the thyroid cells.
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10

Zeng, Wenping, Canjun Li, Ruikun Wu, Xingguo Yang, Qingyan Wang, Bingqian Lin, Yanan Wei, et al. "Optogenetic manipulation of lysosomal physiology and autophagy-dependent clearance of amyloid beta." PLOS Biology 22, no. 4 (April 23, 2024): e3002591. http://dx.doi.org/10.1371/journal.pbio.3002591.

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Lysosomes are degradation centers of cells and intracellular hubs of signal transduction, nutrient sensing, and autophagy regulation. Dysfunction of lysosomes contributes to a variety of diseases, such as lysosomal storage diseases (LSDs) and neurodegeneration, but the mechanisms are not well understood. Altering lysosomal activity and examining its impact on the occurrence and development of disease is an important strategy for studying lysosome-related diseases. However, methods to dynamically regulate lysosomal function in living cells or animals are still lacking. Here, we constructed lysosome-localized optogenetic actuators, named lyso-NpHR3.0, lyso-ArchT, and lyso-ChR2, to achieve optogenetic manipulation of lysosomes. These new actuators enable light-dependent control of lysosomal membrane potential, pH, hydrolase activity, degradation, and Ca2+ dynamics in living cells. Notably, lyso-ChR2 activation induces autophagy through the mTOR pathway, promotes Aβ clearance in an autophagy-dependent manner in cellular models, and alleviates Aβ-induced paralysis in the Caenorhabditis elegans model of Alzheimer’s disease. Our lysosomal optogenetic actuators supplement the optogenetic toolbox and provide a method to dynamically regulate lysosomal physiology and function in living cells and animals.
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Tesis sobre el tema "Lysosomes"

1

Ebrahim, Roshan. "Biogenesis of lysosomes in macrophages : intracellular pathway of lysosomal membrane protein to lysosomes." Doctoral thesis, University of Cape Town, 2008. http://hdl.handle.net/11427/3126.

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Salgues, Frédéric. "Ciblage des lysosomes pour la thérapie enzymatique substitutive ou pour la thérapie photodynamique." Thesis, Montpellier 2, 2011. http://www.theses.fr/2011MON20148.

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Le récepteur du mannose-6-phosphate cation indépendant (RM6P-CI) permet l'endocytose puis le transfert de molécules porteuses du marqueur M6P vers les lysosomes. Pour améliorer à la fois l'affinité pour le RM6P-CI et la stabilité du résidu M6P, nous avons procédé à la synthèse d'analogues isostères stables et fonctionnalisés en position anomère pour permettre un couplage efficace à des molécules d'intérêt thérapeutique. Tout d'abord un couplage à des enzymes recombinantes humaines a été réalisé. Le remodelage de la partie oligosaccharidique de l'enzyme lysosomale GAA, dont la déficience est responsable de la maladie de Pompe, a permis de mettre en évidence que la néoglycoGAA est reconnue efficacement par les RM6P-CI et que son activité enzymatique est totalement conservée. Deuxièmement, le couplage de ces analogues du M6P à des porphyrines en vue de la thérapie photodynamique des cancers est envisagé. Le modèle mis au point en série du mannose a permis de valider notre approche de ligation de saccharides à des photosensibilisateurs par des méthodes évitant après couplage les étapes classiques de déprotection des saccharides. L'étude biologique menée sur les porphyrines glycosylées préparées a démontré leur cytotoxicité photoinduite<br>The cation independent mannose-6-phosphate receptor (CI-M6PR) allows the endocytosis and the transfer of molecules bearing the M6P marker to lysosomes. To improve both the affinity for the CI-M6PR and stability of the M6P residue, we carried out the synthesis of isosteric M6P analogues functionalized at the anomeric position to allow efficient coupling to molecules of therapeutic interest. First, the coupling on human recombinant enzymes was performed. The remodelling of the oligosaccharide part of the lysosomal enzyme GAA, whose deficiency is responsible for Pompe disease, helped to highlight the neoglycoGAA is recognized efficiently by CI-M6PR and its enzymatic activity is completely preserved. Second, the coupling of these analogues of M6P to porphyrins for photodynamic therapy of cancer was considered. The model developed in the mannose series has validated our strategy of ligation of saccharides to photosensitizers. The employed methods avoid the conventional steps of deprotection of saccharides after coupling. The biological study with the prepared glycosylporphyrins demonstrated the photoinduced cytotoxicity
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3

Deng, Yuping. "Studies of intraorganelle dynamics : the lysosome, the pre-lysosomal compartment, and the golgi apparatus /." Diss., This resource online, 1991. http://scholar.lib.vt.edu/theses/available/etd-07282008-134815/.

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Boutry, Maxime. "Dysfonctions des lysosomes et neurodégénérescence : l'exemple de la paraplégie spastique de type SPG11." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066295/document.

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Les lysosomes sont importants pour la survie et la fonction des cellules du système nerveux central et en particulier des neurones. Le mécanisme de la reformation des lysosomes est crucial pour maintenir une quantité adéquate de lysosomes fonctionnels dans les cellules. La spatacsine, qui joue un rôle dans le ce mécanisme est impliquée dans la paraplégie spastique de type SPG11 ; une maladie caractérisée par des troubles moteurs et cognitifs sévères. L’utilisation de modèles cellulaires de cette pathologie permet d’étudier les mécanismes physiopathologiques à l’origine d’altérations de la reformation des lysosomes. J’ai montré que la perte de fonction de la spatacsine est responsable de l’accumulation de lipides dans les lysosomes. Ces accumulations sont constituées de gangliosides et de cholestérol et sont présentes dans les autolysosomes perturbant leur recyclage en lysosomes, notamment en empêchant le recrutement de protéines impliquées dans le mécanisme. Les accumulations de gangliosides rendent les neurones à l’exposition au glutamate ce qui suggère que ces altérations pourraient avoir un rôle dans la neurodégénérescence. J’ai aussi montré que l’absence de spatacsine provoque une dérégulation de l’import de Ca2+ extracellulaire par le « store-operated calcium entry » ce qui conduit à altération de l’homéostasie calcique. L’inhibition de l’import de calcium par le SOCE permet de réduire les accumulations de lipides et de rétablir partiellement le recyclage des lysosomes. Ainsi, l’absence de spatacsine induit une altération de l’homéostasie calcique qui participe à l’accumulation de lipides dans le système lysosomal ce qui est délétère pour la survie des neurones<br>Lysosomal dysfunctions are involved in a large number of neurodegenerative diseases highlightingthe crucial function of lysosomes in neuron survival and function. The mechanism of lysosomereformation from autolysosomes allow cells to maintain the ool of functional lysosomes.Disruptions of this rocess are involved in athologies affecting the central nervous system. Inparticular, spatacsin that lays a role in lysosome recycling is implicated in hereditary spasticparaplegia type SPG11, a severe disease characterized by motors and cognitive alterations. Thispathology is caused by loss of function mutations in SPG11, encoding spatacsin. The study ofSPG11 cellular models gives the opportunity to decipher the hysiopathological mechanismsunderlying lysosomal reformation disruptions.During my thesis, I showed that loss of spatacsin function induces lipid accumulation in lysosomesand articularly in autolysosomes both in fibroblasts and neurons from Spg11-/- mice. Gangliosidesand cholesterol are among lipids that accumulate in autolysosomes impairing lysosomal membranerecycling by disrupting the recruitment of keys roteins. Neurons with ganglioside accumulationsare more sensitive to glutamate induced neuronal death, suggesting that these accumulations areinvolved in neurodegeneration. These results could be of great importance since accumulations ofgangliosides in lysosomes arise in many diseases.I also showed that loss of spatacsin disrupts extracellular calcium import by the store-operatedcalcium entry (SOCE) leading to an increase in cytosolic calcium levels. Lysosomal calcium contentis also increased in Spg11-/- cells and calcium release from lysosome by TRPML1 is reduced.Inhibiting SOCE and stimulating lysosomal calcium release by TRPML1 reduced lipidsaccumulations in lysosomes and artially restored lysosome reformation.Our data suggest that absence of spatacsin is responsible for a disruption of calcium homeostasisthat contributes to lipid accumulation in autolysosomes, disturbing reformation of lysosomes fromautolysosomes. Inhibiting gangliosides synthesis could be used as a therapeutic strategy. However,understanding how loss of function of spatacsin alters these cellular athways will allow thedevelopment of targeted therapeutic approaches
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5

Moule, Christie Joy. "The synthesis and kinetic studies of substrate analogues for N-acetylgalactosamine-4-sulfatase." Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phm926.pdf.

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Piccolo, Enzo. "Rôle de la protéine HMGB1 dérivée des macrophages au cours d'une réaction inflammatoire." Thesis, Toulouse 3, 2021. http://www.theses.fr/2021TOU30035.

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La réaction inflammatoire est la première étape nécessaire pour restaurer l'homéostasie tissulaire lésée. Elle implique au cours de ses différentes étapes, le système immunitaire, notamment les macrophages qui présentent alors divers remaniements inflammatoires et métaboliques. Les macrophages sont capables de modifier et d'adapter leur métabolisme cellulaire afin de satisfaire leurs besoins énergétiques et réaliser de façon efficace la réaction inflammatoire en fonction des signaux du milieu environnant. Ces adaptations métaboliques influencent la physiologie des mitochondries et les oxydations phosphorylantes (OXPHOS), les sécrétions de molécules pro- et antiinflammatoires, ainsi que la capacité à réaliser la phagocytose (pathogènes, débris cellulaire, autophagie) dépendante de la physiologie des lysosomes. Ces adaptations métaboliques sont sous le contrôle de plusieurs facteurs de transcriptions comme NFkB, TFEB ou HIF1alpha. La compaction et l'accessibilité de la chromatine sont des éléments cruciaux pour la régulation indirecte de l'activité de ces facteurs de transcription. Dans le noyau, la compaction de l'ADN est régulée par les histones mais aussi par d'autres protéines de la famille des High Mobility Group (HMG). Parmi les protéines HMG, la protéine High Mobility Group B1 (HMGB1) principalement localisée dans le noyau est capable de réguler de façon indirecte la transcription de gènes dans de nombreux tissus. En plus de son rôle nucléaire, HMGB1 peut être activement relocalisé dans le cytoplasme puis sécrété par les cellules de l'immunité innée au cours d'inflammation aiguë ou chronique. Une fois dans la circulation sanguine HMGB1 joue le rôle d'alarmine qui initie et maintient l'inflammation. De plus, chez la souris au cours d'une inflammation aiguë ou chronique les concentrations d'HMGB1 circulant sont augmentées par rapport à la condition basale. Tous ces résultats suggèrent un rôle d'HMGB1 dans l'immunométabolisme des macrophages ainsi que dans les processus inflammatoires aiguës ou chroniques. Dans ce contexte, ce travail de thèse s'articule autour de deux objectifs : I/: Étudier le rôle d'HMGB1 dérivé des macrophages et de ses conséquences sur la survenue de la fibrose. II/: Étudier le rôle intracellulaire d'HMGB1 dérivé des macrophages au cours du choc inflammatoire aigu. Ces travaux ont permis de démontrer in vitro et in vivo qu'en tant qu'alarmine HMGB1 dérivé des macrophages n'a pas d'influence sur la survenue de la fibrose suite à une nécro-inflammation chronique. De plus, ces travaux ont permis de démontrer in vitro et in vivo qu'en tant que facteur nucléaire, HMGB1 exerce un puissant effet antiinflammatoire en favorisant la polarisation de type M2, en jouant notamment sur la biogénèse et la fonction des lysosomes. Tous ces résultats pris ensemble ont permis de mieux caractériser et comprendre les fonctions biologiques de la protéine HMGB1 dérivée des macrophages au cours du choc inflammatoire aigu. Ce travail permet aussi de mieux envisager des approches thérapeutiques autour de la fonction d'HMGB1 afin d'éviter toute hyper-réaction inflammatoire aux effets délétères pour l'organisme chez des patients atteints de pathologies inflammatoires aiguës/chroniques<br>The Inflammatory reaction is the first necessary step to combat all pathogens and tissue injuries and restore damaged tissue homeostasis. The immune system is particularly involved during each step, in particular the macrophages which display various inflammatory and metabolic changes. Macrophages can modify and adapt their cellular metabolism to meet their energy needs and efficiently perform the inflammatory reaction according to signals from the surrounding environment. These deep metabolic adaptations influence mitochondria physiology and oxidative phosphorylations (OXPHOS), the secretions of pro and anti-inflammatory molecules, as well as the ability to phagocytize various inflammatory compounds (pathogens, cell debris, and autophagy). These deep metabolic adaptations are under the control of several transcription factors such as NFkB, TFEB or HIF1alpha. The compaction and accessibility of chromatin are crucial for the regulation of the activity of these transcription factors. In the nucleus, DNA compaction is regulated by histones but also by High Mobility Group (HMG) proteins. Among this family of HMG proteins, the High Mobility Group B1 (HMGB1) protein, mainly located in the nucleus, is capable of regulating indirectly the transcription of genes in many tissues. In addition to its nuclear role, HMGB1 can be actively relocated into the cytoplasm and then secreted by innate immune cells during acute or chronic inflammation. Once in the bloodstream, HMGB1 acts as alarmine which initiates and maintains inflammation. Furthermore, during acute or chronic inflammation, concentrations of circulating HMGB1 are increased compared to the basal condition in mice. All these results suggest a role of HMGB1 in the immunometabolism of macrophages as well as in acute or chronic inflammatory processes. In this context, this thesis work has two objectives: I /: To study the role of HMGB1 derived from macrophages and its consequences on the occurrence of tissue fibrosis. II /: To study the intracellular role of HMGB1 derived from macrophages during acute inflammatory shock. This work has demonstrated in vitro and in vivo that, as an alarmine HMGB1 derived from macrophages, does not influence the occurrence of fibrosis following chronic inflammation. Moreover, we demonstrated in vitro and in vivo that as a nuclear factor HMGB1 exerts a potent anti-inflammatory action on macrophages by regulating lysosome biogenesis and function and skewing towards a M2 profile. All these results taken together helped to better characterize and understand the biological functions of HMGB1 proteins during the inflammatory reaction. Boosting these anti-inflammatory functions of HMGB1 may constitute a potential therapeutic approach to counteract the deleterious effect of hyper-inflammation in patients with acute/chronic inflammatory diseases
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7

Kågedal, Katarina. "Cathepsin D released from lysosomes mediates apoptosis /." Linköping : Univ, 2003. http://www.bibl.liu.se/liupubl/disp/disp2003/med771s.pdf.

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8

Selmi, Samia. "Études biochimiques et fonctionnelles des lysosomes thyroïdiens." Lyon 1, 1989. http://www.theses.fr/1989LYO1T049.

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Jakhria, Toral Chandulal. "Amyloid fibrils are nanoparticles that target lysosomes." Thesis, University of Leeds, 2014. http://etheses.whiterose.ac.uk/7628/.

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The amyloidoses are a group of debilitating disorders which include neurodegenerative diseases such as Alzheimer’s disease and systemic diseases such as dialysis-related amyloidosis (DRA). Amyloidoses are associated with the aggregation of proteins into amyloid fibrils with a highly organised cross-β structure. Amyloid fibrils are formed by a variety of proteins and peptides despite differences in sequence and native structure. Amyloid formation occurs by a nucleated growth mechanism and proceeds via oligomeric intermediates into mature fibrils. Despite intense research, the molecular mechanisms involved in disease pathogenesis remain unclear. This thesis discusses the mechanism by which amyloid fibrils cause cellular disruption. Chapter 3 describes work performed to validate the use of β2-microglobulin (β2m), the protein that self-associates into amyloid fibrils found in DRA deposits, as a model to study amyloidosis. Fragmentation of mature β2m fibrils, increased their internalisation and access to intracellular compartments, and were therefore used to investigate mechanisms of cellular disruption. Building on previous work in the laboratory showing trafficking of β2m fibrils to the lysosome, chapter 4 examined the effect of fragmented fibrils on lysosomal function and demonstrates that fragmented fibrils impair lysosome-mediated degradation of endocytosed proteins. Following on from this, chapter 5 discusses the effect of fragmented fibrils on membrane trafficking. Fragmented fibrils perturbed the trafficking of lysosomal membrane proteins and also reduced the trafficking of endocytosed cargo to lysosomes. This may rationalise the impairment in degradation of endocytosed proteins. The molecular chaperone, heat shock protein 70 (Hsp70) has been shown to be protective in amyloid disease. The role of Hsp70 in fibril-mediated cell disruption was investigated in chapter 6. Hsp70 protected fibril-treated cells from impairment in degradation of endocytosed protein but not from membrane trafficking defects. This work demonstrates that fragmented fibrils are nanoparticles which target lysosomes and implicates the lysosome in the pathogenesis of amyloidosis.
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Atakpa, Peace. "Ca2+ signalling between the endoplasmic reticulum and lysosomes." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/288002.

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Ca2+ is a universal and versatile intracellular messenger, regulating a vast array of biological processes due to variations in the frequency, amplitude, spatial and temporal dynamics of Ca2+ signals. Increases in cytosolic free Ca2+ concentration ([Ca2+]c) are due to influx from either an infinite extracellular Ca2+ pool or from the more limited intracellular Ca2+ stores. Stimulation of the endogenous muscarinic (M3) receptors of human embryonic kidney (HEK) cells with carbachol results in the activation of phospholipase C (PLC) and formation of inositol 1,4,5-trisphosphate (IP3), activation of IP3 receptors (IP3Rs), release of Ca2+ from the endoplasmic reticulum (ER), and activation of store-operated Ca2+ entry (SOCE). Lysosomes are the core digestive compartments of the cell, but their importance as signalling organelles is also now widely appreciated. Accumulating evidence indicates that lysosomal Ca2+ is important for their physiological functions. Lysosomal Ca2+ release triggers fusion during membrane trafficking and, through calmodulin, it regulates lysosome size. Luminal Ca2+ is critical for regulation of lysosomal biogenesis and autophagy during starvation through the transcription factor, TFEB. Furthermore, aberrant lysosomal Ca2+ is associated with some lysosomal storage diseases. Lysosomes in mammalian cells have long been suggested to accumulate Ca2+ via a low-affinity Ca2+-H+ exchanger (CAX). This is consistent with evidence that dissipating the lysosomal H+ gradient increased [Ca2+]c and decreased lysosomal free [Ca2+], and with the observation that lysosomal Ca2+ uptake was followed by an increase in pHly. Furthermore, heterologous expression of Xenopus CAX in mammalian cells attenuated carbachol-evoked Ca2+ signals. However, there is no known CAX in mammalian cells, and so the identity of the lysosomal Ca2+ uptake pathway in mammalian cells is unresolved. Using mammalian cells loaded with a fluorescent Ca2+ indicator, I show that dissipating the pHly gradient pharmacologically or by siRNA-mediated knockdown of an essential subunit of the H+ pump, increases the amplitude of IP3-evoked cytosolic Ca2+ signals without affecting those evoked by SOCE. A genetically encoded low-affinity Ca2+ sensor expressed on the lysosome surface reports larger increases in [Ca2+]c than the cytosolic sensor, but only when the Ca2+ signals are evoked by IP3R rather than SOCE. Using cells expressing single IP3R subtypes, I demonstrate that each of the three IP3R subtypes can deliver Ca2+ to lysosomes. I conclude that IP3Rs release Ca2+ within near-lysosome microdomains that fuel a low-affinity lysosomal Ca2+ uptake system. The temporal relationship between the increase in pHly and reduced Ca2+ sequestration suggests that pHly affects the organization of the microdomain rather than the Ca2+ uptake mechanism. I show that abrogation of the lysosome H+ gradient does not acutely prevent uptake of Ca2+ into lysosomes, but disrupts junctions with the ER where the exchange of Ca2+ occurs. The dipeptide, glycyl-L-phenylalanine 2-naphthylamide (L-GPN), is much used to disrupt lysosomes and release Ca2+ from them. The mechanism is widely assumed to require cleavage of GPN by cathepsin C, causing accumulation of amino acid residues, and osmotic lysis of lysosomal membranes. I show, using LysoTracker Red and Oregon Green-dextran to report pHly, that L-GPN is effective in HEK cells lacking functional cathepsin C, following CRISPR-Cas9-mediated gene disruption. Furthermore, D-GPN, which is resistant to cleavage by cathepsin C, is as effective as L-GPN at increasing pHly, and it is similarly effective in cells with and without cathepsin C. L-GPN and D-GPN increase cytosolic pH, and the effect is similar when the lysosomal V-ATPase is inhibited with bafilomycin A1. This is not consistent with GPN releasing the acidic contents of lysosomes. I conclude that the effects of GPN on lysosomes are not mediated by cathepsin C. Both L-GPN and D-GPN evoke Ca2+ release, the response is unaffected by inhibition or knock-out of cathepsin C, but it requires Ca2+ within the ER. GPN-evoked increases in [Ca2+]c require Ca2+ within the ER, but they are not mediated by ER Ca2+ channels amplifying Ca2+ release from lysosomes. GPN increases [Ca2+]c by increasing pHcyt, which then directly stimulates Ca2+ release from the ER. I conclude that physiologically relevant increases in pHcyt stimulate Ca2+ release from the ER independent of IP3 and ryanodine receptors, and that GPN does not selectively target lysosomes. I conclude that all three IP3R subtypes selectively deliver Ca2+ to lysosomes, and that the low pH within lysosomes is required to maintain the junctions between ER and lysosomes, but not for lysosomal Ca2+ uptake. I suggest that GPN lacks the specificity required to allow selective release of Ca2+ from lysosomes.
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Libros sobre el tema "Lysosomes"

1

Holtzman, Eric. Lysosomes. New York: Plenum Press, 1989.

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2

Öllinger, Karin, and Hanna Appelqvist, eds. Lysosomes. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6934-0.

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Holtzman, Eric. Lysosomes. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4.

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Holtzman, Eric. Lysosomes. New York: Plenum Press, 1989.

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5

Mehta, Atul B., and Bryan Winchester. Lysosomal storage disorders: A practical guide. Chichester, West Sussex: Wiley-Blackwell, 2013.

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6

Maxfield, Frederick R., James M. Willard, and Shuyan Lu, eds. Lysosomes: Biology, Diseases, and Therapeutics. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118978320.

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7

G, Thoene Jess, ed. Pathophysiology of lysosomal transport. Boca Raton: CRC Press, 1992.

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8

Reunov, A. V. Liticheskai︠a︡ funkt︠s︡ii︠a︡ kletki. Moskva: Nauka, 2008.

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9

Lin, Yuxi. Role of Lysosomes in Nonshivering Thermogenesis. [New York, N.Y.?]: [publisher not identified], 2016.

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10

H, Glaumann, and Ballard F. J, eds. Lysosomes: Their role in protein breakdown. London: Academic Press, 1987.

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Capítulos de libros sobre el tema "Lysosomes"

1

Kuma, Akiko, and Tamotsu Yoshimori. "Pathways to Repair or Remove Lysosomes Damaged by Extracellular Fine Particles." In Extracellular Fine Particles, 169–84. Singapore: Springer Nature Singapore, 2025. https://doi.org/10.1007/978-981-97-7067-0_13.

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Abstract Exogenous and endogenous fine particles such as environmental materials (e.g., silica, asbestos, alum), toxic protein aggregates (e.g., α-synuclein, amyloid-β), and endogenous crystals (e.g., cholesterol crystals, uric acid crystals) are internalized into the cell by the endocytic pathway or phagocytosis. Because lysosomes are the terminal compartments of these pathways, lysosomes are known to be damaged by exocytosed extracellular fine particles. Lysosomal membrane damage allows the leakage of the lysosomal contents such as cathepsins, H+, Ca2+, and iron into the cytosol, which is harmful to the cell. Numerous studies have suggested that lysosomal damage is tightly associated with toxicity of exogenous particles, inflammatory responses, and diseases including those involving neurodegeneration. To preserve lysosomal integrity, cells have several mechanisms for the repair or elimination of compromised lysosomes collectively called the “lysosomal damage response”. This review summarizes recent findings on the responses to lysosomal damage, focusing on extracellular fine particles.
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2

Holtzman, Eric. "Historical Fragments; Methods; Some Terminology." In Lysosomes, 1–24. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_1.

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Holtzman, Eric. "Endocytosis and Heterophagy." In Lysosomes, 25–92. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_2.

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Holtzman, Eric. "Acidification; Membrane Properties; Permeability and Transport." In Lysosomes, 93–160. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_3.

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Holtzman, Eric. "Uses and Abuses of Endocytotic and Heterophagic Pathways." In Lysosomes, 161–241. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_4.

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Holtzman, Eric. "Autophagy and Related Phenomena." In Lysosomes, 243–318. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_5.

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Holtzman, Eric. "Extensive Release. Excessive Storage." In Lysosomes, 319–61. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_6.

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Holtzman, Eric. "Genesis." In Lysosomes, 363–418. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_7.

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Valk, Jacob, and Marjo S. van der Knaap. "Lysosomes and Lysosomal Disorders." In Magnetic Resonance of Myelin, Myelination, and Myelin Disorders, 66–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-02568-0_6.

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Wevers, R. A., and V. Gieselmann. "Lysosomes and Lysosomal Disorders." In Magnetic Resonance of Myelination and Myelin Disorders, 66–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-27660-2_5.

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Actas de conferencias sobre el tema "Lysosomes"

1

Giugliano, Giusy, Michela Schiavo, Daniele Pirone, Jaromir Behal, Vittorio Bianco, Sandro Montefusco, Pasquale Memmolo, Lisa Miccio, Pietro Ferraro, and Diego L. Medina. "Investigation on lysosomal accumulation by a quantitative analysis of 2D phase-maps in digital holography microscopy." In Digital Holography and Three-Dimensional Imaging, Th2A.6. Washington, D.C.: Optica Publishing Group, 2024. http://dx.doi.org/10.1364/dh.2024.th2a.6.

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Quantitative Phase Imaging through Digital Holography (QPI-DH) represents a quantitative and label-free method to detect lysosomal dysfunction in cells. Testing in the cellular model of Mucopolysaccharidosis type III-A, a lysosomal storage disease, demonstrate its potential.
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2

Zhu, X. "Relationship Between Autophagy-Lysosomes Pathway and Ventilator-Induced Diaphragmatic Dysfunction." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2622.

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Perera, Rushika M. "Abstract I22: New players and unique features of cancer lysosomes." In Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; September 6-9, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.panca19-i22.

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Bakhit, C., D. Lewis, R. Billings, and B. Malfroy. "CELLULAR CATABOLISM OF RECOMBINANT TISSUE-TYPE PLASMINOGEN ACTIVATOR: IDENTIFICATION AND CHARACTERIZATION OF A NOVEL HIGH AFFINITY UPTAKE SYSTEM ON RAT HEPATOCYTES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644400.

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The uptake, internalization and intracellular degradation of 125I-labeled rt-PA (125I-rt-PA) by isolated rat hepatocytes was investigated. Incubation at 37°C resulted in internalization of 125I-rt-PA, followed by the appearance of labeled trichloroacetic acid-soluble (TCA) material in the inclubation media due to degradation of rt-PA. Degradation of rt-PA was inhibited by the presence of NH4Cl (10mM) or chloroquine (ImM) (lysosoma tropic agents) in the incubation media. This suggests that rt-PA degradation occurs intracellularly, perhaps within the lysosomes. 125I-rt-PA was taken up by rat hepatocytes through a specific, high affinity mechanism. Scatchard analysis of the data indicated that 106 molecules of rt-PA were taken up per cell/hour and the calculated dissociation constant was lOnM. Uptake of 125I-rt-PA was not inhibited by glycopeptides isolated from rt-PA nor by several other glycoproteins known to be cleared by identified hepatic receptors. These results suggest that the uptake of rt-PA by rat hepatocytes involves a receptor specific for t-PA and is not mediated by a carbohydrate specific receptor.
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Hung, Hsin-I., Geraldine Quiogue, John J. Lemasters, and Anna-Liisa Nieminen. "Signaling from lysosomes to mitochondria sensitizes cancer cells to photodynamic treatment." In SPIE BiOS, edited by David H. Kessel and Tayyaba Hasan. SPIE, 2011. http://dx.doi.org/10.1117/12.878306.

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Quiogue, Geraldine, Shalini Saggu, Hsin-I. Hung, Malcolm E. Kenney, Nancy L. Oleinick, John J. Lemasters, and Anna-Liisa Nieminen. "Signaling from lysosomes enhances mitochondria-mediated photodynamic therapy in cancer cells." In 12th World Congress of the International Photodynamic Association, edited by David H. Kessel. SPIE, 2009. http://dx.doi.org/10.1117/12.823752.

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Joncour, Vadim Le, Pauliina Filppu, Minna Holopainen, Maija Hyvönen, S. Pauliina Turunen, Harri Sihto, Isabel Burghardt, et al. "Abstract LB-055: Novel therapeutic option targeting the tumor cell lysosomes." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-lb-055.

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Tang, Hao-yang, Meng Qian, Cong Song, and Yi-chao Zhang. "Lysosomes Computational Labeling Method Based on Feature Map Slice of Deeplabv3+." In 2019 IEEE Symposium Series on Computational Intelligence (SSCI). IEEE, 2019. http://dx.doi.org/10.1109/ssci44817.2019.9002802.

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Nieminen, Anna-Liisa, Kashif Azizuddin, Ping Zhang, Malcolm E. Kenney, Peter Pediaditakis, John J. Lemasters, and Nancy L. Oleinick. "Contribution of mitochondria and lysosomes to photodynamic therapy-induced death in cancer cells." In Biomedical Optics (BiOS) 2008, edited by David Kessel. SPIE, 2008. http://dx.doi.org/10.1117/12.767356.

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Metelitsina, Irina P., and N. F. Leus. "Action of low-energy monochromatic coherent light on the stability of retinal lysosomes." In Photonics West '95, edited by Steven L. Jacques. SPIE, 1995. http://dx.doi.org/10.1117/12.209925.

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Informes sobre el tema "Lysosomes"

1

Levenson, Victor V. Lysosome-mediated Cell Death and Autophagy-Dependent Multidrug Resistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2008. http://dx.doi.org/10.21236/ada495800.

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Shiio, Yuzuru. Targeting Androgen Receptor by Lysosomal Degradation in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada612607.

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Shiio, Yuzuru. Targeting Androgen Receptor by Lysosomal Degradation in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2015. http://dx.doi.org/10.21236/ada621824.

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Palmer, Guy, Varda Shkap, Wendy Brown, and Thea Molad. Control of bovine anaplasmosis: cytokine enhancement of vaccine efficacy. United States Department of Agriculture, March 2007. http://dx.doi.org/10.32747/2007.7695879.bard.

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Anaplasmosis an arthropod-born disease of cattle caused by the rickettsia Anaplasma marginale and is an impediment to efficient production of healthy livestock in both Israel and the United States. Currently the only effective vaccines are derived from the blood of infected cattle. The risk of widespread transmission of both known and newly emergent pathogens has prevented licensure of live blood-based vaccines in the U.S. and is a major concern for their continued use in Israel. Consequently development of a safe, effective vaccine is a high priority. In this collaborative project we focused on two approaches to vaccine development. The first focused o n improving antigen delivery to livestock and specifically examined how DNA vaccines could be improved to enhance priming and expansion of the immune response. This research resulted in development and testing of two novel vaccine delivery systems--one that targeted antigen spread among dendritic cells (the key cell in priming immune responses and a follow-on construct that also specifically targeted antigen to the endosomal-lysosomal compartment the processing organelle within the dendritic cell that directs vaccine antigen to the MHC class ll-CD4* T cell priming pathway). The optimized construct targeting vaccine antigen to the dendritic cell MHC class II pathway was tested for ability to prime A. marginale specific immune responses in outbred cattle. The results demonstrated both statistically significant effects of priming with a single immunization, continued expansion of the primary immune response including development of high affinity lgG antibodies and rapid recall of the memory response following antigen challenge. This portion of the study represented a significant advance in vaccine delivery for livestock. Importantly the impact of these studies is not limited to A. marginale a s the targeting motifs are optimized for cattle and can be adapted to other cattle vaccinations by inserting a relevant pathogen-specific antigen. The second approach (which represented an addition to the project for which approval was requested as part of the first annual report) was a comparative approach between A . marginale and the Israel A . centrale vaccines train. This addition was requested as studies on Major Surface Protein( MSP)- 2 have shown that this antigen is highly antigenically variable and presented solely as a "static vaccine" antigen does not give cross-strain immunity. In contrast A. . centrale is an effective vaccine which Kimron Veterinary institute has used in the field in Israel for over 50 years. Taking advantage of this expertise, a broad comparison of wild type A. marginale and vaccine strain was initiated. These studies revealed three primary findings: i) use of the vaccine is associated with superinfection, but absence of clinical disease upon superinfection with A. marginale; ii) the A. centrale vaccine strain is not only less virulent but transmission in competent in Dermacentor spp. ticks; and iii) some but not all MSPs are conserved in basic orthologous structure but there are significant polymorphisms among the strains. These studies clearly indicated that there are statistically significant differences in biology (virulence and transmission) and provide a clear path for mapping of biology with the genomes. Based on these findings, we initiated complete genome sequencing of the Israel vaccine strain (although not currently funded by BARD) and plant to proceed with a comparative genomics approach using already sequenced wild-type A. marginale. These findings and ongoing collaborative research tie together filed vaccine experience with new genomic data, providing a new approach to vaccine development against a complex pathogen.
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