L'amélioration des plantes tropicales

L'amélioration des plantes a connu au cours des dix dernières années une évolution rapide. D'une part, elle bénéficie désormais des outils biotechnologiques d'exploitation des ressources génétiques et de création de variétés, qui viennent enrichir les méthodes classiques de sélection. D'autre part, elle doit répondre à de nouvelles attentes : gérer la biodiversité et concourir à une agriculture durable. Cet ouvrage présente les derniers progrès réalisés en amélioration des plantes tropicales. Il se fonde principalement sur les travaux que les équipes françaises du CIRAD et de l'ORSTOM conduisent en collaboration avec leurs homologues des pays tropicaux. Il comprend vingt-quatre chapitres, chacun étant consacré à une culture et rédigé par des spécialistes de la génétique et de la sélection de l'espèce. Pour chaque plante ou groupe de plantes, les auteurs analysent la diversité des formes cultivées et leurs relations avec les espèces sauvages apparentées. Ils décrivent les méthodes d'amélioration et les apports des biotechnologies dans la pratique du sélectionneur. Ils examinent les progrès génétiques réalisés en partant d'exemples tirés des programmes de création variétale. Enfin ils traitent de la diffusion des variétés améliorées. Cet ouvrage de référence s'adresse au chercheur, à l'enseignant, à l'étudiant comme au professionnel de la sélection. (Résumé d'auteur

Localization of HIV-1 Vpr to the nuclear envelope: Impact on Vpr functions and virus replication in macrophages

<p>Abstract</p> <p>Background</p> <p>HIV-1 Vpr is a dynamic protein that primarily localizes in the nucleus, but a significant fraction is concentrated at the nuclear envelope (NE), supporting an interaction between Vpr and components of the nuclear pore complex, including the nucleoporin hCG1. In the present study, we have explored the contribution of Vpr accumulation at the NE to the Vpr functions, including G2-arrest and pro-apoptotic activities, and virus replication in primary macrophages.</p> <p>Results</p> <p>In order to define the functional role of Vpr localization at the NE, we have characterized a set of single-point Vpr mutants, and selected two new mutants with substitutions within the first α-helix of the protein, Vpr-L23F and Vpr-K27M, that failed to associate with hCG1, but were still able to interact with other known relevant host partners of Vpr. In mammalian cells, these mutants failed to localize at the NE resulting in a diffuse nucleocytoplasmic distribution both in HeLa cells and in primary human monocyte-derived macrophages. Other mutants with substitutions in the first α-helix (Vpr-A30L and Vpr-F34I) were similarly distributed between the nucleus and cytoplasm, demonstrating that this helix contains the determinants required for localization of Vpr at the NE. All these mutations also impaired the Vpr-mediated G2-arrest of the cell cycle and the subsequent cell death induction, indicating a functional link between these activities and the Vpr accumulation at the NE. However, this localization is not sufficient, since mutations within the C-terminal basic region of Vpr (Vpr-R80A and Vpr-R90K), disrupted the G2-arrest and apoptotic activities without altering NE localization. Finally, the replication of the Vpr-L23F and Vpr-K27M hCG1-binding deficient mutant viruses was also affected in primary macrophages from some but not all donors.</p> <p>Conclusion</p> <p>These results indicate that the targeting of Vpr to the nuclear pore complex may constitute an early step toward Vpr-induced G2-arrest and subsequent apoptosis; they also suggest that Vpr targeting to the nuclear pore complex is not absolutely required, but can improve HIV-1 replication in macrophages.</p

Genomic Diversity of the Ostreid Herpesvirus Type 1 Across Time and Location and Among Host Species

The mechanisms underlying virus emergence are rarely well understood, making the appearance of outbreaks largely unpredictable. This is particularly true for pathogens with low per-site mutation rates, such as DNA viruses, that do not exhibit a large amount of evolutionary change among genetic sequences sampled at different time points. However, whole-genome sequencing can reveal the accumulation of novel genetic variation between samples, promising to render most, if not all, microbial pathogens measurably evolving and suitable for analytical techniques derived from population genetic theory. Here, we aim to assess the measurability of evolution on epidemiological time scales of the Ostreid herpesvirus 1 (OsHV-1), a double stranded DNA virus of which a new variant, OsHV-1 μVar, emerged in France in 2008, spreading across Europe and causing dramatic economic and ecological damage. We performed phylogenetic analyses of heterochronous (n = 21) OsHV-1 genomes sampled worldwide. Results show sufficient temporal signal in the viral sequences to proceed with phylogenetic molecular clock analyses and they indicate that the genetic diversity seen in these OsHV-1 isolates has arisen within the past three decades. OsHV-1 samples from France and New Zealand did not cluster together suggesting a spatial structuration of the viral populations. The genome-wide study of simple and complex polymorphisms shows that specific genomic regions are deleted in several isolates or accumulate a high number of substitutions. These contrasting and non-random patterns of polymorphism suggest that some genomic regions are affected by strong selective pressures. Interestingly, we also found variant genotypes within all infected individuals. Altogether, these results provide baseline evidence that whole genome sequencing could be used to study population dynamic processes of OsHV-1, and more broadly herpesviruses

Characterization of the Molecular Determinants of Primary HIV-1 Vpr Proteins: Impact of the Q65R and R77Q Substitutions on Vpr Functions

Although HIV-1 Vpr displays several functions in vitro, limited information exists concerning their relevance during infection. Here, we characterized Vpr variants isolated from a rapid and a long-term non-progressor (LTNP). Interestingly, vpr alleles isolated from longitudinal samples of the LTNP revealed a dominant sequence that subsequently led to diversity similar to that observed in the progressor patient. Most of primary Vpr proteins accumulated at the nuclear envelope and interacted with host-cell partners of Vpr. They displayed cytostatic and proapoptotic activities, although a LTNP allele, harboring the Q65R substitution, failed to bind the DCAF1 subunit of the Cul4a/DDB1 E3 ligase and was inactive. This Q65R substitution correlated with impairment of Vpr docking at the nuclear envelope, raising the possibility of a functional link between this property and the Vpr cytostatic activity. In contradiction with published results, the R77Q substitution, found in LTNP alleles, did not influence Vpr proapoptotic activity

HIV-1 Vpr-Induced Apoptosis Is Cell Cycle Dependent and Requires Bax but Not ANT

The HIV-1 accessory protein viral protein R (Vpr) causes G(2) arrest and apoptosis in infected cells. We previously identified the DNA damage–signaling protein ATR as the cellular factor that mediates Vpr-induced G(2) arrest and apoptosis. Here, we examine the mechanism of induction of apoptosis by Vpr and how it relates to induction of G(2) arrest. We find that entry into G(2) is a requirement for Vpr to induce apoptosis. We investigated the role of the mitochondrial permeability transition pore by knockdown of its essential component, the adenine nucleotide translocator. We found that Vpr-induced apoptosis was unaffected by knockdown of ANT. Instead, apoptosis is triggered through a different mitochondrial pore protein, Bax. In support of the idea that checkpoint activation and apoptosis induction are functionally linked, we show that Bax activation by Vpr was ablated when ATR or GADD45α was knocked down. Certain mutants of Vpr, such as R77Q and I74A, identified in long-term nonprogressors, have been proposed to inefficiently induce apoptosis while activating the G(2) checkpoint in a normal manner. We tested the in vitro phenotypes of these mutants and found that their abilities to induce apoptosis and G(2) arrest are indistinguishable from those of HIV-1(NL4–3) vpr, providing additional support to the idea that G(2) arrest and apoptosis induction are mechanistically linked

Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome associated with COVID-19: An Emulated Target Trial Analysis.

RATIONALE: Whether COVID patients may benefit from extracorporeal membrane oxygenation (ECMO) compared with conventional invasive mechanical ventilation (IMV) remains unknown. OBJECTIVES: To estimate the effect of ECMO on 90-Day mortality vs IMV only Methods: Among 4,244 critically ill adult patients with COVID-19 included in a multicenter cohort study, we emulated a target trial comparing the treatment strategies of initiating ECMO vs. no ECMO within 7 days of IMV in patients with severe acute respiratory distress syndrome (PaO2/FiO2 <80 or PaCO2 ≥60 mmHg). We controlled for confounding using a multivariable Cox model based on predefined variables. MAIN RESULTS: 1,235 patients met the full eligibility criteria for the emulated trial, among whom 164 patients initiated ECMO. The ECMO strategy had a higher survival probability at Day-7 from the onset of eligibility criteria (87% vs 83%, risk difference: 4%, 95% CI 0;9%) which decreased during follow-up (survival at Day-90: 63% vs 65%, risk difference: -2%, 95% CI -10;5%). However, ECMO was associated with higher survival when performed in high-volume ECMO centers or in regions where a specific ECMO network organization was set up to handle high demand, and when initiated within the first 4 days of MV and in profoundly hypoxemic patients. CONCLUSIONS: In an emulated trial based on a nationwide COVID-19 cohort, we found differential survival over time of an ECMO compared with a no-ECMO strategy. However, ECMO was consistently associated with better outcomes when performed in high-volume centers and in regions with ECMO capacities specifically organized to handle high demand. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives License 4.0 (http://creativecommons.org/licenses/by-nc-nd/4.0/)

Rôle de la protéine virale Vpr dans les étapes précoces du cycle réplicatif du VIH-1 (étude des interactions Vpr/hCG1 et hCG1/dynamitine)

PARIS-BIUP (751062107) / SudocSudocFranceF

Hétérogénéité et fonctions des lymphocytes B chez l’homme

L’étude de l’expression de différents marqueurs membranaires permet de délimiter plusieurs sous-populations de lymphocytes B, qui jouent des rôles distincts dans la réponse immunitaire humorale. En outre, les lymphocytes B possèdent des fonctions indépendantes de la production d’anticorps. Produits tout au long de la vie par la moelle osseuse, où s’effectuent les réarrangements des gènes d’immunoglobulines au cours des étapes de maturation des précurseurs de la lignée B, les lymphocytes B naïfs co-expriment des IgM et des IgD membranaires (IgMlow IgDhigh) qui constituent leur récepteur pour l’antigène (BcR), et sont susceptibles de s’orienter vers différentes voies de différenciation conduisant à la mise en place de sous-populations distinctes

Effects of propiconazole on extra-cellular enzymes involved in nutrient mobilization during Trametes versicolor wood colonization

International audienceThe effects of propiconazole on extra-cellular enzyme levels in Trametes versicolor have been investigated during wood colonization and degradation. The working hypothesis was that the biocide could alter metabolic pathways, which could lead to an alteration of extra-cellular enzyme production. In the presence of a propiconazole sub-lethal concentration, the wood degradation rate decrease concomitantly with the lag phase of fungal development observed during wood colonisation. The pattern of production of enzymes involved in polysaccharide degradation (b-glucosidases, glucuronidases, cellobiohydrolases), nitrogen (leucine aminopeptidase) and phosphorus (acid phosphatase) mobilization was only slightly altered in the presence of the biocide. In experiments performed in the presence of propiconazole, there was a strong induction of chitinases at the beginning of the colonization process. Addition of caffeine, a pleiotropic drug, which is also a chitinase inhibitor, together with propiconazole resulted in synergistic inhibition of the fungal growth. The implication of these results in the development of a new wood preservation strategy is discussed

Effect of heat treatment on extracellular enzymatic activities involved in beech wood degradation by Trametes versicolor

International audienc