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Isogenic bar-coded strains of Aspergillus fumigatus carrying the G54W or M220K mutation in Cyp51A were constructed. In vitro , the growth and conidiation capacities of the mutants were similar to those of the parental strain. Competition studies in the absence of azoles showed that there was no adverse fitness cost for the azole-resistant A. fumigatus strains in vitro or in vivo compared to the parental strain.

Introduction Aspergillus fumigatus est un champignon saprophyte present de facon ubiquitaire dans l’environnement. L’inhalation des spores est a l’origine de reactions pulmonaires allergiques severes chez certains sujets. Chez les individus sains, l’elimination du champignon implique l’activation du systeme immunitaire inne, notamment via les macrophages alveolaires, responsables du developpement d’une reponse immunitaire rapide et non specifique, et par les neutrophiles, qui reconnaissent plus specifiquement les tubes germinatifs du champignon. L’epithelium bronchique, premiere barriere naturelle et premier element de defense des voies aeriennes superieures vis-a-vis des pathogenes aeroportes est implique dans la clairance mucociliaire mais represente egalement la cible d’une exposition par voie inhalee a A. fumigatus . Ce projet vise a determiner le role de la cellule epitheliale bronchique dans la reponse initiale a l’infection par A. fumigatus . Methodes Nous avons developpe un modele d’infection d’un epithelium bronchique humain differencie, se rapprochant des conditions physiopathologiques chez l’homme. Pour cela, des cellules epitheliales bronchiques humaines primaires (HBECs) sont mises en contact avec des spores issues d’une culture sur gelose d’ A. fumigatus . Aux differents temps d’infection, une mesure de la resistance trans-epitheliale est realisee, ainsi que l’extraction ARN pour une etude de l’expression des cytokines en PCR quantitative. Resultats Nous avons observe une internalisation des conidies par les HBECs lorsqu’elles sont cultivees en monocouche, mais non lorsqu’elles sont cultivees en ALI. L’exposition des HBECs differenciees a A. fumigatus est cependant associee a la production de cytokines pro-inflammatoires (IL-6 et IL-1s). De plus, A. umigatus induit une perte de l’integrite de l’epithelium, tel que mis en evidence par une chute de la resistance electrique trans-epitheliale de l’epithelium des 8 heures post-infection. Conclusions La colonisation des voies respiratoires par A. fumigatus n’impliquerait pas l’internalisation des conidies par les cellules epitheliales bronchiques. L’epithelium bronchique jouerait un role de barriere physique lors de l’infection par A. fumigatus , mais egalement de sentinelle de part la synthese de cytokines stimulant le recrutement des cellules immunitaires.

International audience; 3-Aminopropyl α-(1→3)-pentaglucoside, a fragment of α-(1→3)-glucan of the cell wall of Aspergillus fumigatus, has been synthesized in a blockwise approach. The application of mono- and disaccharide N-phenyltrifluoroacetimidates bearing a stereodirecting 6-O-benzoyl group was essential for stereoselective α-glucosylations. In the products, p-methoxyphenyl and levulinoyl groups served as orthogonal protecting groups for the anomeric position and 3-OH group, respectively. Their removal from shared blocks led to donors and acceptors that were used for the synthesis of pentasaccharides. Coupling of free α-(1→3)-pentaglucoside with biotin and bovine serum albumin (BSA) gave glycoconjugate tools for mycological studies. Immunization of mice with the BSA conjugate induced the generation of antibodies that recognize α-(1→3)-glucan on A. fumigatus cell wall and distinguish its morphotypes. This discovery represents a first step to the development of a diagnostic test system and a vaccine to detect and fight this life-threatening pathogen.

Protein phosphatases Z that are unique to the fungal kingdom have been associated to resistance to high salt concentration, cell wall integrity, cell cycle regulation, and oxidative stress in fungi. In Aspergillus fumigatus, it was shown that PHZA is under the control of the transcription factor Skn7 and is only involved in the control of the oxidative stress. Accordingly, the ΔphzA mutant showed a defect in virulence in an experimental model of corneal infection in immunocompetent animals and that the impact on susceptibility to cell wall drugs is only secondary.

CORRIGENDUM: Circulating human basophils lack the features of professional antigen presenting cells

The choline oxidase ( CHOA ) and betaine aldehyde dehydrogenase ( BADH ) genes identified in Aspergillus fumigatus are present as a cluster specific for fungal genomes. Biochemical and molecular analyses of this cluster showed that it has very specific biochemical and functional features that make it unique and different from its plant and bacterial homologs. A. fumigatus ChoAp catalyzed the oxidation of choline to glycine betaine with betaine aldehyde as an intermediate and reduced molecular oxygen to hydrogen peroxide using FAD as a cofactor. A. fumigatus Badhp oxidized betaine aldehyde to glycine betaine with reduction of NAD + to NADH. Analysis of the AfchoA Δ:: HPH and AfbadA Δ:: HPH single mutants and the AfchoA Δ AfbadA Δ:: HPH double mutant showed that Af ChoAp is essential for the use of choline as the sole nitrogen, carbon, or carbon and nitrogen source during the germination process. Af ChoAp and Af BadAp were localized in the cytosol of germinating conidia and mycelia but were absent from resting conidia. Characterization of the mutant phenotypes showed that glycine betaine in A. fumigatus functions exclusively as a metabolic intermediate in the catabolism of choline and not as a stress protectant. This study in A. fumigatus is the first molecular, cellular, and biochemical characterization of the glycine betaine biosynthetic pathway in the fungal kingdom.

International audience; BACKGROUND:SUN proteins are involved in yeast morphogenesis, but their function is unknown.RESULTS:SUN protein plays a role in the Aspergillus fumigatus morphogenesis. Biochemical properties of recombinant SUN proteins were elucidated.CONCLUSION:Both Candida albicans and Aspergillus fumigatus sun proteins show a β-(1,3)-glucanase activity.SIGNIFICANCE:The mode of action of SUN proteins on β-(1,3)-glucan is unique, new, and original. In yeasts, the family of SUN proteins has been involved in cell wall biogenesis. Here, we report the characterization of SUN proteins in a filamentous fungus, Aspergillus fumigatus. The function of the two A. fumigatus SUN genes was investigated by combining reverse genetics and biochemistry. During conidial swelling and mycelial growth, the expression of AfSUN1 was strongly induced, whereas the expression of AfSUN2 was not detectable. Deletion of AfSUN1 negatively affected hyphal growth and conidiation. A closer examination of the morphological defects revealed swollen hyphae, leaky tips, intrahyphal growth, and double cell wall, suggesting that, like in yeast, AfSun1p is associated with cell wall biogenesis. In contrast to AfSUN1, deletion of AfSUN2 either in the parental strain or in the AfSUN1 single mutant strain did not affect colony and hyphal morphology. Biochemical characterization of the recombinant AfSun1p and Candida albicans Sun41p showed that both proteins had a unique hydrolysis pattern: acting on β-(1,3)-oligomers from dimer up to insoluble β-(1,3)-glucan. Referring to the CAZy database, it is clear that fungal SUN proteins represent a new family of glucan hydrolases (GH132) and play an important morphogenetic role in fungal cell wall biogenesis and septation.

International audience; Recent reports in mice demonstrate that basophils function as antigen presenting cells (APC). They express MHC class II and co-stimulatory molecules CD80 and CD86, capture and present soluble antigens or IgE-antigen complexes and polarize Th2 responses. Therefore, we explored whether human circulating basophils possess the features of professional APC. We found that unlike dendritic cells (DC) and monocytes, steady-state circulating human basophils did not express HLA-DR and co-stimulatory molecules CD80 and CD86. Basophils remained negative for these molecules following stimulation with soluble Asp f 1, one of the allergens of Aspergillus fumigatus; Bet v 1, the major birch allergen; TLR2-ligand or even upon IgE cross-linking. Unlike DC, Asp f 1-pulsed basophils did not promote Th2 responses as analyzed by the secretion of IL-4 in the basophil-CD4+ T cell co-culture. Together, these results demonstrate the inability of circulating human basophils to function as professional APC.

Aspergillus fumigatus is a model fungal pathogen and a common cause of infection in individuals with the primary immunodeficiency chronic granulomatous disease (CGD). Although primarily considered a deficiency of innate immunity, CGD is also linked to dysfunctional T cell reactivity. Both CD4+ and CD8+ T cells mediate vaccine-induced protection from experimental aspergillosis, but the molecular mechanisms leading to the generation of protective immunity and whether these mechanisms are dysregulated in individuals with CGD have not been determined. Here, we show that activation of either T cell subset in a mouse model of CGD is contingent upon the nature of the fungal vaccine, the involvement of distinct innate receptor signaling pathways, and the mode of antigen routing and presentation in DCs. Aspergillus conidia activated CD8+ T cells upon sorting to the Rab14+ endosomal compartment required for alternative MHC class I presentation. Cross-priming of CD8+ T cells failed to occur in mice with CGD due to defective DC endosomal alkalinization and autophagy. However, long-lasting antifungal protection and disease control were successfully achieved upon vaccination with purified fungal antigens that activated CD4+ T cells through the endosome/lysosome pathway. Our study thus indicates that distinct intracellular pathways are exploited for the priming of CD4+ and CD8+ T cells to A. fumigatus and suggests that CD4+ T cell vaccination may be able to overcome defective antifungal CD8+ T cell memory in individuals with CGD., The studies were supported by the Specific Targeted Research Projects ‘‘ALLFUN’’ (FP7_HEALTH_2009_260338), the Italian Projects AIDS 2010 by ISS (Istituto Superiore di Sanità — contract number 40H40), and 2011.0124.021 RICERCA SCIENTIFICA E TECNOLOGICA by Fondazione Cassa di Risparmio di Perugia, all to to L. Romani.

Aspergillus fumigatus has two chitin synthases ( CSMA and CSMB ) with a myosin motor-like domain (MMD) arranged in a head-to-head configuration. To understand the function of these chitin synthases, single and double csm mutant strains were constructed and analyzed. Although there was a slight reduction in mycelial growth of the mutants, the total chitin synthase activity and the cell wall chitin content were similar in the mycelium of all of the mutants and the parental strain. In the conidia, chitin content in the Δ csmA strain cell wall was less than half the amount found in the parental strain. In contrast, the Δ csmB mutant strain and, unexpectedly, the Δ csmA /Δ csmB mutant strain did not show any modification of chitin content in their conidial cell walls. In contrast to the hydrophobic conidia of the parental strain, conidia of all of the csm mutants were hydrophilic due to the presence of an amorphous material covering the hydrophobic surface-rodlet layer. The deletion of CSM genes also resulted in an increased susceptibility of resting and germinating conidia to echinocandins. These results show that the deletion of the CSMA and CSMB genes induced a significant disorganization of the cell wall structure, even though they contribute only weakly to the overall cell wall chitin synthesis.

Aspergillus fumigatus is the most common and deadly pulmonary fungal infection worldwide. In the lung, the fungus usually forms a dense colony of filaments embedded in a polymeric extracellular matrix. To identify candidate genes involved in this biofilm (BF) growth, we used RNA-Seq to compare the transcriptomes of BF and liquid plankton (PL) growth. Sequencing and mapping of tens of millions sequence reads against the A. fumigatus transcriptome identified 3,728 differentially regulated genes in the two conditions. Although many of these genes, including the ones coding for transcription factors, stress response, the ribosome, and the translation machinery, likely reflect the different growth demands in the two conditions, our experiment also identified hundreds of candidate genes for the observed differences in morphology and pathobiology between BF and PL. We found an overrepresentation of upregulated genes in transport, secondary metabolism, and cell wall and surface functions. Furthermore, upregulated genes showed significant spatial structure across the A. fumigatus genome; they were more likely to occur in subtelomeric regions and colocalized in 27 genomic neighborhoods, many of which overlapped with known or candidate secondary metabolism gene clusters. We also identified 1,164 genes that were downregulated. This gene set was not spatially structured across the genome and was overrepresented in genes participating in primary metabolic functions, including carbon and amino acid metabolism. These results add valuable insight into the genetics of biofilm formation in A. fumigatus and other filamentous fungi and identify many relevant, in the context of biofilm biology, candidate genes for downstream functional experiments.

We recently reported on DprA and DprB, dehydrin-like proteins involved in the protection against oxidative, osmotic and pH stress in Aspergillus fumigatus. A third dehydrin-like gene, DprC, was detected in the genome of the filamentous fungus and repressed during conidial germination. The deletion mutant was impaired in freezing tolerance. The DprC-mediated response was dependent on the SakA MAP kinase pathway, and accordingly, SakA phosphorylation was induced by cold shock. When fused to eGFP, the protein was associated with the vacuoles.

MgtC is important for the survival of several bacterial pathogens in macrophages and for growth under magnesium limitation. Among eukaryotes, a gene homologous to mgtC was found only in the pathogenic fungus Aspergillus fumigatus . Our data show that the A. fumigatus MgtC (AfuMgtC) protein does not have the same function as the bacterial MgtC proteins.

This article identifies novel stress-protective proteins that belong to the family of intrinsically unstructured proteins, DprA and DprB, which are associated with the cytosol and the peroxisomes in Aspergillus fumigatus., During a search for genes controlling conidial dormancy in Aspergillus fumigatus, two dehydrin-like genes, DprA and DprB, were identified. The deduced proteins had repeated stretches of 23 amino acids that contained a conserved dehydrin-like protein (DPR) motif. Disrupted DprAΔ mutants were hypersensitive to oxidative stress and to phagocytic killing, whereas DprBΔ mutants were impaired in osmotic and pH stress responses. However, no effect was observed on their pathogenicity in our experimental models of invasive aspergillosis. Molecular dissection of the signaling pathways acting upstream showed that expression of DprA was dependent on the stress-activated kinase SakA and the cyclic AMP-protein kinase A (cAMP-PKA) pathways, which activate the bZIP transcription factor AtfA, while expression of DprB was dependent on the SakA mitogen-activated protein kinase (MAPK) pathway, and the zinc finger transcription factor PacC. Fluorescent protein fusions showed that both proteins were associated with peroxisomes and the cytosol. Accordingly, DprA and DprB were important for peroxisome function. Our findings reveal a novel family of stress-protective proteins in A. fumigatus and, potentially, in filamentous ascomycetes.

International audience; Reactive oxidant species produced by phagocytes have been reported as being involved in the killing of Aspergillus fumigatus. Fungal superoxide dismutases (SODs) that detoxify superoxide anions could be putative virulence factors for this opportunistic pathogen. Four genes encoding putative Sods have been identified in the A. fumigatus genome: a cytoplasmic Cu/ZnSOD (AfSod1p), a mitochondrial MnSOD (AfSod2p), a cytoplasmic MnSOD (AfSod3p) and AfSod4 displaying a MnSOD C-terminal domain. During growth, AfSOD1 and AfSOD2 were highly expressed in conidia whereas AfSOD3 was only strongly expressed in mycelium. AfSOD4 was weakly expressed compared with other SODs. The deletion of AfSOD4 was lethal. Delta sod1 and Delta sod2 mutants showed a growth inhibition at high temperature and a hypersensitivity to menadione whereas the sod3 mutant had only a slight growth delay at high temperature. Multiple mutations had only an additive effect on the phenotype. The triple sod1/sod2/sod3 mutant was characterized by a delay in conidial germination, a reduced conidial survival during storage overtime, the highest sensitivity to menadione and an increased sensitivity to killing by alveolar macrophage of immunocompetent mice. In spite of these phenotypes, no significant virulence difference was observed between the triple mutant and parental strain in experimental murine aspergillosis models in immunocompromised animals.

International audience; P>Galactofuranose (Galf) is a major molecule found in cell wall polysaccharides, secreted glycoproteins, membrane lipophosphoglycans and sphingolipids of Aspergillus fumigatus. The initial step in the Galf synthetic pathway is the re-arrangement of UDP-galactopyranose to UDP-Galf through the action of UDP-galactopyranose mutase. A mutant lacking the AfUGM1 gene encoding the UDP-galactopyranose mutase has been constructed. In the mutant, though there is a moderate reduction in the mycelial growth associated with an increased branching, it remains as pathogenic and as resistant to cell wall inhibitors and phagocytes as the wild-type parental strain. The major phenotype seen is a modification of the cell wall surface that results in an increase in adhesion of the mutants to different inert surfaces (glass and plastic) and epithelial respiratory cells. The adhesive phenotype is due to the unmasking of the mannan consecutive to the removal of galactofuran by the ugm1 mutation. Removal of the mannan layer from the mutant surface by a mannosidase treatment abolishes mycelial adhesion to surfaces.

Abstract 3229 Introduction: Several studies have reported that different components of fungi of the genera Aspergillus spp may induce protective T-cell responses in either mouse models of invasive aspergillosis (IA) or in human healthy subjects. We evaluated the occurrence of Aspergillus-specific T-cell responses to different Aspergillus recombinant antigens in patients with proven IA, during the course of the IA, to identify the antigens most frequently targeted by protective immune responses. We characterized phenotypically and functionally such specific T cells. Finally, from peripheral blood (PB) samples of the same IA proven patients, also collected during the active infection phase, we sought to expand such Aspergillus-specific T cells. Methods: 15 patients with proven IA, according to the EORTC/MSG criteria, have been enrolled into the study. Specific immune responses producing interleukin-10 (IL-10), interferon-gamma (IFN-γ), IL-4 and IL-17A were detected and characterized by enzyme linked immunospot (ELISpot) assay and cytokine secretion assay (CSA), in all the patients, during the entire course of the IA. The recombinant antigens used were GEL1p, CRF1p, PEP1p, SOD1p, α1–3glucan, β1–3glucan, and galactomannan (GM). Cytotoxicity has been investigated by means of the colorimetric assay with (2,3-bis[2-methoxy-4-nitro-5-sulfophenyl]2H-tetrazolium-5-carboxyanilide) sodium salt plus coenzyme Q0 (XTT assay). Aspergillus-specific T cells were obtained by culturing PB mononuclear cells with a mixture containing PEP1p, GEL1p, α1–3 glucan and β1–3 glucan. The infection course were divided into 4 phases, defined from t1 to t4, each of fifteen days interval, starting from the radiological diagnosis of IA. Results: Aspergillus-specific T cells producing either IL-10 or IFN-γ were detected to all the antigens, but GM. The number of antigens targeted by IFN-γ producing specific T cells progressively increased along the course of IA, being such protective responses to 3 out of 7 antigens at t1 and to 6 out of 7 antigens at t4. At t1, IFN-γ producing specific T cells were only detected to GEL1p, α1–3 glucan and β1–3 glucan. GEL1p and α1–3 glucan resulted the antigens most constantly targeted by IFN-γ producing specific T cells, persisting the responses to these antigens in all the phases of IA. No Aspergillus-specific T cells producing IL-4 to any antigens were detected by the ELISpot assay. Aspergillus-specific T cells producing IL-17A were detected in only one out of 15 patients, and targeted CRF1p. Specific T cells to GM and specific T cells producing IL-4 to all the antigens could be shown only by CSA, suggesting that they are present only at very low frequencies during the infection. After 13-day cultures, Aspergillus-specific T cells were expanded from five out of five patients. The specific T cells tested for lytic activity included a median of 95.8% CD3+ cells, either CD4+ or CD8+ T cells, and showed a median lytic activity of 9.45% either at 3/1 or at 5/1 effector/target cells ratios. Conclusions: In patients with IA, protective immune responses may be detected since the onset and increase during the infection. At the onset of IA, specific T cells producing IFN-γ target antigens involved in the cell wall biosynthesis of Aspergillus. On the other hand, at the same phase, specific protective immune responses to CRF1p, PEP1p, and SOD1p, which are all putative virulence factors for Aspergillus, are absent. Aspergillus-specific T cells may be expanded by a mixture of antigens, even in the course of IA and are able to directly kill fungal hyphae. The above mentioned antigens and the corresponding protective T cells may be exploited for therapeutic strategies of either vaccine or autologous cytotoxic cell infusions in patients at high risk for IA. Disclosures: Luppi: MSD; GILEAD: Research Funding.

Since the 1970s, environmental philosophy has been mainly concerned with the intrinsic value of nature and with the preservation of some rare and remarkable forms of nature which stand in remote areas. Influenced by the American classical idea of wilderness, which excludes humans from nature, environmental philosophers worked to elaborate intrinsic value theories of nature. By doing so, they suggested that nature had disappeared from the human inhabited world, i.e. from almost the whole Earth. Against this idea, I argue for nature being part of our societies. Humans and nature share a living mutual interdependence. Following this hypothesis, we will see how natural beings could be considered partners in most of our productive and reproductive activities, while we often act wrongly with these members of our communities. That's why there is a need for an ethics of everyday nature.; Depuis les années 1970, les philosophies environnementales se sont essentiellement préoccupées de la question de la valeur morale de la nature rare et remarquable, qui subsiste dans quelques régions de la planète. Héritant de la pensée américaine de la wilderness, les philosophes de l'environnement se sont efforcés de donner des fondations théoriques à la valeur intrinsèque d'une nature, dont l'homme se devait d'être absent. Ce faisant, ils laissaient à penser que sur les terres habitées ou transformées par les hommes, qui couvrent la quasi-totalité de la surface de la planète, il fallait renoncer à penser la nature. À rebours de cette idée, nous soutenons qu'il y a de la nature dans les sociétés humaines, que nous faisons société avec la nature. En suivant cette hypothèse, nous ferons apparaître, à partir d'un matériau descriptif varié, que nos activités productives et reproductives engagent, en effet, de nombreux acteurs naturels, mais aussi que, très souvent, nous nous conduisons mal avec ces derniers. C'est ce qui nous semble motiver l'élaboration d'une éthique de la nature ordinaire.

International audience

Depuis les années 1970 plusieurs domaines d’expertise scientifique ont contribué à faire émerger une nouvelle dimension de la protection de l’environnement liés aux effets dégradants de la pollution lumineuse. Cette dernière constitue en soi un objet de controverse entre sciences, notamment sur les différentes façons de la saisir et la définir en tant qu’objet et que fait. Nous retiendrons ici pour qualifier cette forme de pollution le caractère d’un excès de lumière artificielle entrainant des impacts sur les écosystèmes et sur la santé humaine. L’histoire du mouvement de lutte contre l’expansion de l’éclairage artificiel commence à être relativement connue, dans le monde et en France. Les sciences écologiques et médicales ont progressivement constitué des champs de savoirs scientifiques relatifs aux effets et impacts négatifs de l’éclairage artificiel sur les écosystèmes et la santé, qui ont permis la reconnaissance de la pollution lumineuse comme nouveau problème environnemental. Dans cette « contestation » de la lumière, elles ont rejoint les astronomes professionnels et amateurs qui ont été les premiers à dénoncer les impacts socioculturels de l’éclairage artificiel nocturne, en mettant en exergue la perte du rapport à la nuit entendue comme ressource complexe aux dimensions tout à la fois culturelles, philosophiques, scientifiques, ou encore paysagères. La question de la « sauvegarde de la nuit » émerge comme enjeu d’action publique en France dans les années 1990 avec la constitution d’un mouvement de mobilisation qui se structure à travers l’ANPCEN (Association nationale pour la protection du ciel et de l’environnement nocturne). C’est au cours des années 2000 que se dessine une première fenêtre d’opportunité politique pour ce mouvement. Le contexte de difficultés budgétaires des collectivités territoriales et la nécessité de plus en plus pressante d’une transition énergétique au regard du réchauffement climatique amènent à considérer différemment la fabrique de l’éclairage urbain. Les postures des éclairagistes évoluent et un nombre croissant de communes adoptent des politiques de réduction des niveaux d’éclairement, voire des coupures de l’éclairage public durant certaines plages horaires.Suite au Grenelle de l’Environnement, la prévention des nuisances lumineuse se traduit par la création d’un nouveau chapitre réglementaire au sein du Code de l’environnement. Ces dispositions définissent les installations lumineuses et les équipements concernés, ainsi que les différents types de zones sur lesquelles les prescriptions seront déclinées pour tenir compte des enjeux du territoire concerné, normalisant ainsi l’éclairage dans l’espace. La construction de ce champ réglementaire de protection de la nuit se poursuit, à travers différentes étapes. Dans le même temps, des dispositifs de labellisation de démarches territoriales sont élaborés et mis en oeuvre. Les labels "étoilés" dont le plus connu est celui de la « Réserve Internationale de Ciel Étoilé » (RICE) de l’International Dark sky Association (IDA) sont en fait des certifications internationales. Ce label RICE apparaît en France en décembre 2013, à l’occasion de la labellisation de la première réserve française autour du Pic du Midi de Bigorre et de son observatoire (Bourgeois et Charlier, 2013). Cette première labellisation permet à la France de rejoindre un mouvement qui a alors déjà touché les pays anglo-saxons et plusieurs pays européens. Une autre dynamique de labellisation très importante existe depuis 2009 à l’échelle des communes, celui des « Villes et Villages Étoilés » de l’ANPCEN. Cette démarche, soutenue par France Nature Environnement, la Fédération des PNR, encourage la maîtrise des dépenses d’énergie et les extinctions de l’éclairage public. Dans le domaine de l’écologie et de la géographie de la conservation, l’expérimentation enfin de méthodologies essayant d’articuler dynamiques des espèces et aménagement du territoire a ouvert un autre chapitre de la mise en protection de la nuit à travers le concept de « trame noire ». Fondé sur le principe de la mise en place de maillages de continuités écologiques, la construction hypothétique de cet outil encourage les recherches sur la fragmentation écologique des milieux par la lumière artificielle (effets et impacts écologiques de la lumière, notamment sur les processus de déplacement, de migrations, de prédation et de reproduction). Du ciel étoilé des astronomes aux « corridors noirs » des écologues, la protection de la nuit et de l’environnement nocturne revêtent des déclinaisons plurielles (socioculturelles, écologiques et sanitaires) et s’incarne dans des démarches dont les méthodologies sont parfois encore peu éprouvées. Elle n’en est pas moins un sujet bénéficiant d’un réel effet de mode et l’organisation en novembre 2018 par le Parc national des Cévennes d’un colloque dédié à « la protection et la valorisation de l’environnement nocturne » marque la pleine maturité de cette dynamique. Qu’on la qualifie par la perte de patrimoine, la dégradation d’habitats, les effets perturbateurs voire destructeurs sur les espèces, ou bien la construction potentielle de ressources pour l’action collective locale, l’appropriation de cette thématique de protection par les réseaux d’aires protégées est pleinement en cours.

International audience; « Bas carbone », « Zéro carbone » sont quelques-uns des slogans réitérés dans les discussions et les négociations climatiques. Qu’un élément abondant, aussi omniprésent et familier que le carbone puisse devenir la source de tous les maux n’est pas l’un des moindres paradoxes de l’Anthropocène. En effet, on désigne le carbone comme l’ennemi à abattre, au sens littéral de « mettre à terre ». Parmi tous les gaz à effet de serre, il est celui qu’il faut « capturer », « séquestrer », « neutraliser », etc. L’empreinte carbone est comme une souillure qu’il s’agirait d’effacer. Parce que le dioxyde de carbone résulte d’une combustion, il met l’accent sur le choix du feu comme péché originel sur lequel notre civilisation serait bâtie. Ainsi, plus que tout autre gaz, il connecte la problématique du réchauffement climatique avec celle de notre dépendance aux énergies fossiles. Pourtant, si le carbone est la menace, il est aussi considéré comme fournissant des clés sinon des solutions. Ainsi l’impératif écologique « décarboner » est-il assorti de dispositifs de mesure tels que le bilan carbone, et de transactions financières telles que la compensation carbone et les échanges de crédits carbone. Or ces dispositifs se basent sur le choix du carbone comme étalon de mesure ou parangon de tous les gaz à effet de serre. Le carbone offre ainsi prise à la quantification. Il fournit un équivalent général et fonctionne comme un outil de régulation des échanges entre les humains et la planète. Mais ce Janus a bien d’autres faces et fonctions. Car le carbone est polymorphe et manifestement pluriel. Après avoir souligné la portée culturelle du carbone, on montrera que prendre en compte les multiples modes d’existence du carbone est essentiel pour échapper au piège du temps unique qu’entretient le concept d’Anthropocène. En effet, l’idée d’une collusion entre le temps long de la géologie et le temps court de la civilisation industrielle suggère certes un brouillage d’échelles mais ne remet pas en cause le postulat d’un temps unique et linéaire. L’Anthropocène perpétue la flèche du temps et nourrit les complaintes actuelles au sujet de l’accélération. Ce faisant, il entretient et même renforce l’affrontement entre techno-optimistes et techno-catastrophistes. Or les multiples modes d’existence du carbone nous apprennent justement qu’il n’y a pas un temps unique. Non seulement notre vision linéaire du temps s’accommode mal du temps cyclique du carbone au travers des sols, de l’atmosphère, des océans et du vivant, mais aussi elle esquive les effets intriqués et parfois antagonistes des cycles du carbone. Les cycles multiples du carbone remettent en cause la vision d’un monde bien ordonné, où tout est commensurable, avec des ordres de grandeur sagement emboîtés depuis les constituants ultimes de l’atome jusqu’aux montagnes et aux volcans. Il s’agit donc de penser carbones (au pluriel) et d’agir dans un monde aux temporalités multiples, bref d’affronter la difficulté de penser, de prévoir et d’agir en polychronie.

International audience; Premier paragraphe de l'articlePeut-on dépasser la nature par le droit ? L’anthropocentrisme suffit-il à penser l’Anthropocène ? C’est à travers le droit international que ces interrogations seront poussées à leurs extrêmes, voire jusqu’à l’absurde. Plutôt que d’opposer ou de séparer l’homme et la nature, envisageons leurs rapports à travers ceux du droit international et du droit de l’environnement. Réduisons même le droit international à ce temple de l’humanisme qu’est le droit international humanitaire. Peut-on englober l’environnement dans ce droit ? Serait-ce une absorption et une disparition ?On procédera par trois expériences de pensée dont le point commun est de pousser à bout les présupposés anthropocentriques de ce droit. Ces hypothèses mettront en évidence les implicites qui font de la nature un donné, tenu pour acquis et toujours disponible. Supposons que :1.la totalité du droit international humanitaire soit appliquée ;2.toutes les responsabilités dans le réchauffement climatique soient pénalement assignées ;3.supposons enfin un État n’existant que par le droit international

International audience

International audience

International audience; Vezatin, a protein associated to adherens junctions in epithelial cells, is already expressed in mouse oocytes and during pre-implantation development. Using a floxed strategy to generate a vezatin-null allele, we show that the lack of zygotic vezatin is embryonic lethal, indicating that vezatin is an essential gene. Homozygous null embryos are able to elicit a decidual response but as early as day 6.0 post-coitum mutant implantation sites are devoid of embryonic structures. Mutant blastocysts are morphologically normal, but only half of them are able to hatch upon in vitro culture and the blastocyst outgrowths formed after 3.5 days in culture exhibit severe abnormalities, in particular disrupted intercellular adhesion and clear signs of cellular degeneration. Notably, the junctional proteins E-cadherin and beta-catenin are delocalized and not observed at the plasma membrane anymore. These in vitro observations reinforce the idea that homozygous vezatin-null mutants die at the time of implantation because of a defect in intercellular adhesion. Together these results indicate that the absence of zygotic vezatin is deleterious for the implantation process, most likely because cadherin-dependent intercellular adhesion is impaired in late blastocysts when the maternal vezatin is lost.