Pathologie végétale

Résumé

thumb|Pomme de terre infectée par le mildiou (Phytophthora infestans) thumb|Tumeur sur tronc de platane La pathologie végétale, ou phytopathologie ou phytiatrie, est la science qui étudie les maladies des plantes, surtout des plantes cultivées. La distinction entre une maladie et un problème d'ordre physiologique n'est pas toujours facile à établir. À la fin de cet article est placée une énumération de problèmes physiologiques pouvant être confondus avec des maladies. Les maladies des plantes sont dues à divers organismes : champignons, oomycètes, bactéries, virus, viroïdes, phytoplasmes, protozoaires, nématodes et plantes parasites. Toutefois dans la littérature francophone, contrairement à la littérature anglophone, les nématodes ne sont pas inclus dans les agents infectieux causes de maladies des plantes. Ces organismes sont normalement présents et souvent en grande quantité dans leur environnement, parfois même des organismes utiles ou symbiotes à la plante, et qui se développe

Source officielle

https://fr.wikipedia.org/wiki/Pathologie_v%C3%A9g%C3%A9tale

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Engineering Agrobacterium tumefaciens Adhesion to Target Cells

Zaïnebe Al-Mayyah, Alexandre Louis André Persat, Alix Kim Lan Pham, Xavier Jean-Yves Pierrat, Jeremy Pak Hei Wong

Agrobacterium tumefaciens is a plant pathogen commonly repurposed for genetic modification of crops. Despite its versatility, it remains inefficient at transferring DNA to many hosts, including to animal cells. Like many pathogens, physical contact between A. tumefaciens and host cells promotes infection efficacy. Thus, improving the strength and specificity of A. tumefaciens to target cells has the potential for enhancing DNA transfer for biotechnological and therapeutic purposes. Here, we demonstrate a methodology for engineering genetically encoded exogeneous adhesins at the surface of A. tumefaciens. We identified an autotransporter gene we named Aat that is predicted to show canonical beta-barrel and passenger domains. We engineered the beta-barrel scaffold and linker (Aat(beta)) to display synthetic adhesins susceptible to rewire A. tumefaciens to alternative host targets. As a proof of concept, we leveraged the versatility of a VHH domain to rewire A. tumefaciens adhesion to yeast and mammalian hosts displaying a GFP target receptor. Finally, to demonstrate how synthetic A. tumefaciens adhesion can improve transfer to host cells, we showed improved protein translocation into HeLa cells using a sensitive split luciferase reporter system. Engineering A. tumefaciens adhesion has therefore a strong potential in generating complex heterogeneous cellular assemblies and in improving DNA transfer efficiency against non-natural hosts.

AMER CHEMICAL SOC2022

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Although it has been nearly two and half decades since the discovery of alpha-synuclein (aSyn) as the major component of Lewy bodies (LBs), our understanding of the involvement of different aSyn species, their seeding, spreading and toxicity in Parkinson's disease (PD) is limited. One of the major causes underlying this knowledge gap is the unavailability of adequate tools, techniques, and model systems to capture, monitor, and evaluate the role of different aSyn species in the disease process. In addition, our understanding of cell-type specific contributions to disease pathogenesis is limited. In this thesis, we systematically address the current knowledge gaps and elucidate the structural and cellular determinants of aSyn seeding and toxicity using cellular and animal model systems of PD. In the first chapter of this thesis, we describe an antibody characterization and validation pipeline to assess the specificity of antibodies to well-characterized preparations of various aSyn species, including monomers, fibrils, and different type of oligomers. Using an array of techniques, we demonstrate that that: i) none of the antibodies tested are specific for one particular type of aSyn species, including monomers, oligomers or fibrils; ii) all antibodies that were reported to be oligomer-specific also recognized fibrillar aSyn; and iii) a few antibodies (e.g., the antibody clone 26F1, 5G4) showed high specificity for oligomers and fibrils but did not bind to monomers. These findings suggest that most aSyn aggregate-specific antibodies cannot be used to differentiate between oligomers and fibrils, thus highlighting the importance of exercising caution when interpreting results obtained using these antibodies. In the second chapter of this thesis, we systematically addressed the current knowledge gaps on the role of aSyn oligomers in the initiation, seeding and pathology spreading. Towards this goal, we used different biophysical approaches to investigate aSyn seeding in vitro and in neurons and animal models of aSyn seeding and pathology spreading. we observed that oligomeric forms do not form in the PFF-based neuronal seeding model and we report that different types of oligomers do not seed pathology in vitro and primary hippocampal neurons, and their presence slows rather than accelerates aSyn fibrillization. Altogether, our work points to fibrils as the most seeding competent species and suggests that they are the critical mediators of pathology spreading in PD and other synucleinopathies.In the third chapter of this thesis, we used single-nuclei RNA-sequencing to investigate transcriptional changes in different cell types of the amygdala brain region, which is highly susceptible to developing pS129 positive aggregates in the PD brains. We identified that most of the top 100 differentially expressed genes (DEGs) are of neuronal rather than non-neuronal cell types. In addition, we report that the gene expression profile of a handful of PD risk genes such as Sncaip, Park7, Maob, Hspa8, Scl2a3 and Hsf3 and some pathways that have been associated with PD are differentially altered in specific cell types. Our study highlights the involvement of unique gene expression changes and their associated pathways in different cell types in driving the disease process at an early stage in a PFF-based mouse model of PD.

EPFL2022

Chargement

Opportunities and challenges of alpha-synuclein as a potential biomarker for Parkinson's disease and other synucleinopathies

Hilal Lashuel, Pedro José Santana Ribeiro Magalhães

Parkinson's disease (PD), the second most common progressive neurodegenerative disease, develops and progresses for 10-15 years before the clinical diagnostic symptoms of the disease are manifested. Furthermore, several aspects of PD pathology overlap with other neurodegenerative diseases (NDDs) linked to alpha-synuclein (aSyn) aggregation, also called synucleinopathies. Therefore, there is an urgent need to discover and validate early diagnostic and prognostic markers that reflect disease pathophysiology, progression, severity, and potential differences in disease mechanisms between PD and other NDDs. The close association between aSyn and the development of pathology in synucleinopathies, along with the identification of aSyn species in biological fluids, has led to increasing interest in aSyn species as potential biomarkers for early diagnosis of PD and differentiate it from other synucleinopathies. In this review, we (1) provide an overview of the progress toward mapping the distribution of aSyn species in the brain, peripheral tissues, and biological fluids; (2) present comparative and critical analysis of previous studies that measured total aSyn as well as other species such as modified and aggregated forms of aSyn in different biological fluids; and (3) highlight conceptual and technical gaps and challenges that could hinder the development and validation of reliable aSyn biomarkers; and (4) outline a series of recommendations to address these challenges. Finally, we propose a combined biomarker approach based on integrating biochemical, aggregation and structure features of aSyn, in addition to other biomarkers of neurodegeneration. We believe that capturing the diversity of aSyn species is essential to develop robust assays and diagnostics for early detection, patient stratification, monitoring of disease progression, and differentiation between synucleinopathies. This could transform clinical trial design and implementation, accelerate the development of new therapies, and improve clinical decisions and treatment strategies.

NATURE PORTFOLIO2022

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Opportunities and challenges of alpha-synuclein as a potential biomarker for Parkinson's disease and other synucleinopathies

Hilal Lashuel, Pedro José Santana Ribeiro Magalhães

NATURE PORTFOLIO2022

EPFL2022