22 research outputs found

    SARS-CoV-2 transmission via apical syncytia release from primary bronchial epithelia and infectivity restriction in children epithelia

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    The beta-coronavirus SARS-CoV-2 is at the origin of a persistent worldwide pandemic. SARS-CoV-2 infections initiate in the bronchi of the upper respiratory tract and are able to disseminate to the lower respiratory tract eventually causing acute severe respiratory syndrome with a high degree of mortality in the elderly. Here we use reconstituted primary bronchial epithelia from adult and children donors to follow the infection dynamic following infection with SARS-CoV-2. We show that in bronchial epithelia derived from adult donors, infections initiate in multi-ciliated cells. Then, infection rapidly spread within 24-48h throughout the whole epithelia. Within 3-4 days, large apical syncytia form between multi-ciliated cells and basal cells, which dissipate into the apical lumen. We show that these syncytia are a significant source of the released infectious dose. In stark contrast to these findings, bronchial epithelia reconstituted from children donors are intrinsically more resistant to virus infection and show active restriction of virus spread. This restriction is paired with accelerated release of IFN compared to adult donors. Taken together our findings reveal apical syncytia formation as an underappreciated source of infectious virus for either local dissemination or release into the environment. Furthermore, we provide direct evidence that children bronchial epithelia are more resistant to infection with SARS-CoV-2 providing experimental support for epidemiological observations that SARS-CoV-2 cases’ fatality is linked to age. Significance Statement Bronchial epithelia are the primary target for SARS-CoV-2 infections. Our work uses reconstituted bronchial epithelia from adults and children. We show that infection of adult epithelia with SARS-CoV-2 is rapid and results in the synchronized release of large clusters of infected cells and syncytia into the apical lumen contributing to the released infectious virus dose. Infection of children derived bronchial epithelia revealed an intrinsic resistance to infection and virus spread, probably as a result of a faster onset of interferon secretion. Thus, our data provide direct evidence for the epidemiological observation that children are less susceptible to SARS-CoV-2

    Sea ice diatom contributions to Holocene nutrient utilization in East Antarctica

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    Combined high-resolution Holocene ÎŽ30Sidiat and ÎŽ13Cdiat paleorecords are presented from theSeasonal Ice Zone, East Antarctica. Both data sets reïŹ‚ect periods of increased nutrient utilization by diatomsduring the Hypsithermal period (circa 7800 to 3500 calendar years (cal years) B.P.), coincident with a higherabundance of open water diatom species (Fragilariopsis kerguelensis), increased biogenic silica productivity(%BSi), and higher regional summer temperatures. The Neoglacial period (after circa 3500 cal years B.P.) isreïŹ‚ected by an increase in sea ice indicative species (Fragilariopsis curta and Fragilariopsis cylindrus,upto50%) along with a decrease in %BSi and ÎŽ13Cdiat(< 18‰ to 23‰). However, over this period, ÎŽ30Sidiatdata show an increasing trend, to some of the highest values in the Holocene record (average of +0.43‰).Competing hypotheses are discussed to account for the decoupling trend in utilization proxies including ironfertilization, species-dependent fractionation effects, and diatom habitats. Based on mass balance calculations,we highlight that diatom species derived from the semi-enclosed sea ice environment may have a confoundingeffect upon ÎŽ30Sidowncorecompositions of the seasonal sea ice zone. A diatom composition, with approximately28% of biogenic silica derived from the sea ice environment (diat-SI) can account for the increased averagecompo sition of ÎŽ30Sidiatduring the Neoglacial. These data highlight the signiïŹcant role sea ice diatoms can playwith relation to their export in sediment records, which has implications on productivity reconstructions fromthe seasonal ice zone

    Study of liquid-liquid phase separation and the fact histone chaperone in the adenovirus type 5 replication compartment organization.

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    L’AdĂ©novirus est un virus Ă  ADN double brin qui est utilisĂ© comme vecteur vaccinal. Son gĂ©nome est trĂšs compactĂ© Ă  l’intĂ©rieur de la particule virale et il est organisĂ© en chromatine grĂące Ă  son association avec la protĂ©ine virale VII. La libĂ©ration du gĂ©nome viral dans le noyau d’une cellule cible est suivie par sa dĂ©compaction, par l’éviction partielle de protĂ©ines VII et le dĂ©pĂŽt d’histones cellulaires afin d’initier la transcription des gĂšnes viraux puis la rĂ©plication de l’ADN viral. A un stade plus tardif, ce processus est inversĂ© et les gĂ©nomes viraux sont condensĂ©s et compactĂ©s en chromatine associĂ©e Ă  la protĂ©ine VII et dĂ©pourvue d’histones cellulaires. A l’heure actuelle, peu de facteurs impliquĂ©s dans cette chromatinisation rĂ©versible du gĂ©nome adĂ©noviral sont connus. Ces facteurs sont probablement les chaperons d’histone cellulaires, classĂ©s en trois groupes diffĂ©rents agissant de maniĂšre dĂ©pendante ou non de la rĂ©plication, ou durant la rĂ©paration de l’ADN. La rĂ©plication de l’ADN viral s’effectue Ă  l’intĂ©rieur d’organelles non-membranaires induites par le virus et nommĂ©es compartiments de rĂ©plication viraux (CR). Les CR sont formĂ©s par des facteurs de l’hĂŽte et par des protĂ©ines virales comme la protĂ©ine de rĂ©plication virale DBP (DNA Binding Protein). Les CR sont morphologiquement dynamiques et deux types de CR distincts peuvent ĂȘtre distinguĂ©s. Les CR prĂ©coces sont supposĂ©s rĂ©pliquer les gĂ©nomes pour l’expression des gĂšnes viraux tandis que les CR tardifs entourent des corps appelĂ©s corps viraux induits aprĂšs la rĂ©plication (ViPR bodies en anglais) qui sont le site d’accumulation de gĂ©nomes susceptibles d’ĂȘtre encapsidĂ©s dans les nouvelles particules virales. Nous avons essayĂ© d’élucider le mĂ©canisme Ă  l’origine de la formation des CR et des ViPR et ce qui permet le recrutement ou l’exclusion des protĂ©ines de l’hĂŽte et des protĂ©ines virales, qui pourrait ĂȘtre nĂ©cessaire Ă  la chromatinisation rĂ©versible des gĂ©nomes viraux. Les mĂ©canismes impliquĂ©s sont probablement la sĂ©paration de phase liquide-liquide (LLPS). La LLPS est un processus physique rĂ©versible permettant l’enrichissement et l’appauvrissement en facteurs au sein de deux phases fonctionnelles distinctes formĂ©es par de faibles interactions entre des protĂ©ines et des acides nuclĂ©iques. Elle pourrait expliquer la formation des CR de l’AdĂ©novirus. Dans ce travail, nous avons montrĂ© que les CR sont dĂ©pourvus d’histones cellulaires, qu’ils excluent la chromatine de l’hĂŽte et que des chaperons d’histones incluant FACT (FAcilitates Chromatin Transcription) y sont spĂ©cifiquement associĂ©s. FACT s’accumule dans les CR et sa sous-unitĂ© SSRP1 induit de la sĂ©paration de phase suggĂ©rant un rĂŽle dans la formation des CR de l’AdĂ©novirus et la rĂ©plication et/ou la transcription du gĂ©nome viral probablement par la chromatinisation rĂ©versible du gĂ©nome viral. Ce travail permettra de mieux comprendre le devenir du gĂ©nome adĂ©noviral dans la cellule infectĂ©e et potentiellement d’amĂ©liorer encore les vecteurs basĂ©s sur les AdĂ©novirus.Adenovirus is a double stranded DNA virus which is used as a viral vector vaccine. Its genome is highly compacted inside the viral particle and organized into chromatin by virtue of the protein VII. Nuclear genome delivery in a target cell is followed by decompaction and partial eviction of protein VII and the deposition of cellular histones to initiate viral genes transcription and then the viral DNA replication. At late stages the process is reversed and viral genomes are condensed and packaged into a chromatin associated with proteins VII and without cellular histones. Few factors involved in driving this reversible chromatinization of the adenoviral genome are known. Potential candidates involve cellular histone chaperons, which are classed into three different groups acting replication dependent, replication independent or following DNA repair. Viral genome replication occurs in virus induced membraneless organelles called viral replication compartment (RC) formedwith host factors and viral proteins like the viral DBP (DNA Binding Protein) protein. RCs are morphologically dynamic and two distinct RCs can be distinguished. Early RCs are presumed to replicate genomes for gene expression while late RCs surround bodies called viral induced post replication bodies (ViPR bodies) which are the site of viral genome accumulation likely for their encapsidation into new viral particles. We tried to elucidate the mechanism driving RC and ViPR bodiesformation and what allows the recruitment or exclusion of both host and viral proteins which can be necessary for the reversible viral genome chromatinization. Mechanisms involved are likely liquid-liquid phase separation (LLPS). LLPS is a reversible physical process permitting the enrichment and depletion of factors within two functional separate phases formed by weak interactions between proteins and nucleic acids. It can explain the adenoviral RC formation. In this work, we have shown that RCs are histone free, exclude host chromatin and that histone chaperones including FACT (FAcilitates Chromatin Transcription) are specifically associated with RCs. FACT accumulates in RC and its SSRP1 subunit drives phase separation suggesting a role in Adenovirus RC formation and genome replication and/or transcription possibly by reversible genome chromatinization. This work will allow to better understand the fate of the adenoviral genome in the infected cell and to improve potentially adenoviral based vectors. This thesis work also focused on the study of SARS-CoV-2 which can cause acute respiratory distress syndrome with a high degree of mortality in elderly patients. We established functional reconstitutedprimary bronchial epithelia (BE) derived from donors (adults and children) to study SARS-CoV-2 infection in a physiologically relevant model. We identified multi-ciliated cells as the primary target cells for SARS-CoV-2. We further observed rapid viral spread throughout the entire BE within 24-48 hours. Within 3-4 days, we observed syncytia formation between ciliated cells and basal cells which accumulate at the apical side of the BE. We show that infected cells including syncytia are releasedinto the apical lumen and contribute to the transmittable virus dose. Interestingly, some BE mainly reconstituted from young donor, showed an intrinsic resistance to infection and virus spread. This restricted infection phenotype correlated with a faster release of type-III interferon secretion. Moreover, exogenous type-III interferon treatment to permissive epithelia installed infection restriction while interferon gene knockout promoted infection. Taken together our data uncover syncytia formation as possible contribution to tissue or environmental SARS-CoV-2 dissemination and the type-III IFN response as a central contributor to SARS-CoV-2 resistance in BE, which may explain epidemiological observations that SARS-CoV-2 fatality is age dependent

    Etude de la séparation de phase liquide-liquide et du chaperon d'histone fact dans l'organisation du compartiment de réplication de l'adénovirus de type 5

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    Adenovirus is a double stranded DNA virus which is used as a viral vector vaccine. Its genome is highly compacted inside the viral particle and organized into chromatin by virtue of the protein VII. Nuclear genome delivery in a target cell is followed by decompaction and partial eviction of protein VII and the deposition of cellular histones to initiate viral genes transcription and then the viral DNA replication. At late stages the process is reversed and viral genomes are condensed and packaged into a chromatin associated with proteins VII and without cellular histones. Few factors involved in driving this reversible chromatinization of the adenoviral genome are known. Potential candidates involve cellular histone chaperons, which are classed into three different groups acting replication dependent, replication independent or following DNA repair. Viral genome replication occurs in virus induced membraneless organelles called viral replication compartment (RC) formedwith host factors and viral proteins like the viral DBP (DNA Binding Protein) protein. RCs are morphologically dynamic and two distinct RCs can be distinguished. Early RCs are presumed to replicate genomes for gene expression while late RCs surround bodies called viral induced post replication bodies (ViPR bodies) which are the site of viral genome accumulation likely for their encapsidation into new viral particles. We tried to elucidate the mechanism driving RC and ViPR bodiesformation and what allows the recruitment or exclusion of both host and viral proteins which can be necessary for the reversible viral genome chromatinization. Mechanisms involved are likely liquid-liquid phase separation (LLPS). LLPS is a reversible physical process permitting the enrichment and depletion of factors within two functional separate phases formed by weak interactions between proteins and nucleic acids. It can explain the adenoviral RC formation. In this work, we have shown that RCs are histone free, exclude host chromatin and that histone chaperones including FACT (FAcilitates Chromatin Transcription) are specifically associated with RCs. FACT accumulates in RC and its SSRP1 subunit drives phase separation suggesting a role in Adenovirus RC formation and genome replication and/or transcription possibly by reversible genome chromatinization. This work will allow to better understand the fate of the adenoviral genome in the infected cell and to improve potentially adenoviral based vectors. This thesis work also focused on the study of SARS-CoV-2 which can cause acute respiratory distress syndrome with a high degree of mortality in elderly patients. We established functional reconstitutedprimary bronchial epithelia (BE) derived from donors (adults and children) to study SARS-CoV-2 infection in a physiologically relevant model. We identified multi-ciliated cells as the primary target cells for SARS-CoV-2. We further observed rapid viral spread throughout the entire BE within 24-48 hours. Within 3-4 days, we observed syncytia formation between ciliated cells and basal cells which accumulate at the apical side of the BE. We show that infected cells including syncytia are releasedinto the apical lumen and contribute to the transmittable virus dose. Interestingly, some BE mainly reconstituted from young donor, showed an intrinsic resistance to infection and virus spread. This restricted infection phenotype correlated with a faster release of type-III interferon secretion. Moreover, exogenous type-III interferon treatment to permissive epithelia installed infection restriction while interferon gene knockout promoted infection. Taken together our data uncover syncytia formation as possible contribution to tissue or environmental SARS-CoV-2 dissemination and the type-III IFN response as a central contributor to SARS-CoV-2 resistance in BE, which may explain epidemiological observations that SARS-CoV-2 fatality is age dependent.L’AdĂ©novirus est un virus Ă  ADN double brin qui est utilisĂ© comme vecteur vaccinal. Son gĂ©nome est trĂšs compactĂ© Ă  l’intĂ©rieur de la particule virale et il est organisĂ© en chromatine grĂące Ă  son association avec la protĂ©ine virale VII. La libĂ©ration du gĂ©nome viral dans le noyau d’une cellule cible est suivie par sa dĂ©compaction, par l’éviction partielle de protĂ©ines VII et le dĂ©pĂŽt d’histones cellulaires afin d’initier la transcription des gĂšnes viraux puis la rĂ©plication de l’ADN viral. A un stade plus tardif, ce processus est inversĂ© et les gĂ©nomes viraux sont condensĂ©s et compactĂ©s en chromatine associĂ©e Ă  la protĂ©ine VII et dĂ©pourvue d’histones cellulaires. A l’heure actuelle, peu de facteurs impliquĂ©s dans cette chromatinisation rĂ©versible du gĂ©nome adĂ©noviral sont connus. Ces facteurs sont probablement les chaperons d’histone cellulaires, classĂ©s en trois groupes diffĂ©rents agissant de maniĂšre dĂ©pendante ou non de la rĂ©plication, ou durant la rĂ©paration de l’ADN. La rĂ©plication de l’ADN viral s’effectue Ă  l’intĂ©rieur d’organelles non-membranaires induites par le virus et nommĂ©es compartiments de rĂ©plication viraux (CR). Les CR sont formĂ©s par des facteurs de l’hĂŽte et par des protĂ©ines virales comme la protĂ©ine de rĂ©plication virale DBP (DNA Binding Protein). Les CR sont morphologiquement dynamiques et deux types de CR distincts peuvent ĂȘtre distinguĂ©s. Les CR prĂ©coces sont supposĂ©s rĂ©pliquer les gĂ©nomes pour l’expression des gĂšnes viraux tandis que les CR tardifs entourent des corps appelĂ©s corps viraux induits aprĂšs la rĂ©plication (ViPR bodies en anglais) qui sont le site d’accumulation de gĂ©nomes susceptibles d’ĂȘtre encapsidĂ©s dans les nouvelles particules virales. Nous avons essayĂ© d’élucider le mĂ©canisme Ă  l’origine de la formation des CR et des ViPR et ce qui permet le recrutement ou l’exclusion des protĂ©ines de l’hĂŽte et des protĂ©ines virales, qui pourrait ĂȘtre nĂ©cessaire Ă  la chromatinisation rĂ©versible des gĂ©nomes viraux. Les mĂ©canismes impliquĂ©s sont probablement la sĂ©paration de phase liquide-liquide (LLPS). La LLPS est un processus physique rĂ©versible permettant l’enrichissement et l’appauvrissement en facteurs au sein de deux phases fonctionnelles distinctes formĂ©es par de faibles interactions entre des protĂ©ines et des acides nuclĂ©iques. Elle pourrait expliquer la formation des CR de l’AdĂ©novirus. Dans ce travail, nous avons montrĂ© que les CR sont dĂ©pourvus d’histones cellulaires, qu’ils excluent la chromatine de l’hĂŽte et que des chaperons d’histones incluant FACT (FAcilitates Chromatin Transcription) y sont spĂ©cifiquement associĂ©s. FACT s’accumule dans les CR et sa sous-unitĂ© SSRP1 induit de la sĂ©paration de phase suggĂ©rant un rĂŽle dans la formation des CR de l’AdĂ©novirus et la rĂ©plication et/ou la transcription du gĂ©nome viral probablement par la chromatinisation rĂ©versible du gĂ©nome viral. Ce travail permettra de mieux comprendre le devenir du gĂ©nome adĂ©noviral dans la cellule infectĂ©e et potentiellement d’amĂ©liorer encore les vecteurs basĂ©s sur les AdĂ©novirus

    Experimental Evidence for Seed Metabolic Allometry in Barrel Medic (Medicago truncatula Gaertn.)

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    International audienceSeed size is often considered to be an important trait for seed quality, i.e., vigour and germination performance. It is believed that seed size reflects the quantity of reserve material and thus the C and N sources available for post-germinative processes. However, mechanisms linking seed size and quality are poorly documented. In particular, specific metabolic changes when seed size varies are not well-known. To gain insight into this aspect, we examined seed size and composition across different accessions of barrel medic (Medicago truncatula Gaertn.) from the genetic core collection. We conducted multi-elemental analyses and isotope measurements, as well as exact mass GC–MS metabolomics. There was a systematic increase in N content (+0.17% N mg−1) and a decrease in H content (–0.14% H mg−1) with seed size, reflecting lower lipid and higher S-poor protein quantity. There was also a decrease in 2H natural abundance (ή2H), due to the lower prevalence of 2H-enriched lipid hydrogen atoms that underwent isotopic exchange with water during seed development. Metabolomics showed that seed size correlates with free amino acid and hexoses content, and anticorrelates with amino acid degradation products, disaccharides, malic acid and free fatty acids. All accessions followed the same trend, with insignificant differences in metabolic properties between them. Our results show that there is no general, proportional increase in metabolite pools with seed size. Seed size appears to be determined by metabolic balance (between sugar and amino acid degradation vs. utilisation for storage), which is in turn likely determined by phloem source metabolite delivery during seed development

    Tropical extremes : natural variability and trends

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    The West African Monsoon (WAM) has undergone drastic changes in the recent past causing dramatic impacts on populations. After 30 years of devastating drought, the last two decades experienced a growing number of damaging floods concurrent with ongoing episodes of water shortages and famines. This raised the issue of a more extreme climate in the Sahel with more intense rainfall and dry spells. This chapter gives an overview of progress on documenting the rainfall extremes in the Sahel, a subject that has long been ignored in the literature. It focuses on statistical characteristics of extremes, on their trends in the context of WAM decadal variability and on the physical mechanisms involved in their occurrence. Based on recent literature and original analyses of daily rain gauge records in the central Sahel, a significant intensification of the Sahelian rainfall regime is confirmed over the last 15 years: more extreme events, larger size storms, accompanied by a deficit in the occurrence of less intense events. From a composite of 20 extreme storms in Ouagadougou, some key atmospheric conditions are shown to drive extreme precipitation, including an intense southerly monsoon flux coincident with strong African easterly waves and a large-scale moist anomaly at the regional scale

    Constraining plateau development in southern Africa by combining thermochronology, sediment flux, topography, and landscape evolution modeling

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    International audienceThe southern African Plateau is a dominant feature of African topography but there is considerable debate about when and how it formed. Mantle dynamics have been suggested to play an important role in the topographic evolution, but the time and specific mechanisms of topographic development are still contested. Three main intervals have been proposed for when most of the uplift occurred in southern Africa: 1) it was already elevated at the time of Gondwana breakup at ~150 Ma due to large igneous province activity based on models of rift flank uplift, 2) uplift occurred 100-80 Ma either due to deep mantle or lithospheric processes based on a major erosion phase detected in thermochronology and marine sediment flux, or 3) uplift occurred after ~30 Ma due to small scale convection in the upper mantle based on geomorphic planation surfaces and river profile analysis. Here, we test which of the three intervals of plateau development are plausible using erosion, sedimentation, and topographic data from southern Africa and a landscape evolution model. Recent work from several efforts has provided a clearer picture of the erosion history of the plateau surface and margins using low temperature thermochronology and the geometries of the depositional systems in the surrounding offshore basins. Landscape evolution model results are directly compared with apatite fission track and (U-Th)/He dates from across the plateau, sediment flux volumes in the surrounding marine basins, and present-day topographic metrics. We use an inversion method to constrain the range in erosional and uplift model parameters that can best reproduce the observed data. Results indicate two families of uplift histories are most compatible with the data. Both have limited initial topography and some topographic uplift and continental tilting starting in the east of the continent at ~95 Ma. In one acceptable scenario nearly all of the topography, ~1500 m, is created at this time with very little uplift in the Cenozoic. In the other acceptable scenario, only ~500 m of uplift occurs in the mid-Cretaceous with another ~850 m of uplift in the mid-Cenozoic. The data cannot easily distinguish between these two uplift patterns suggesting different proxies would be helpful to fully constrain the timing of plateau development and any climatic influences on the erosion history

    Constraining plateau uplift in southern Africa by combining thermochronology, sediment flux, topography, and landscape evolution modeling

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    International audienceThe uplift of the southern African Plateau with its average elevations of ~1000 m is often attributed to mantle processes, but there are conflicting theories for the timing and drivers of topographic development. Evidence for most proposed plateau development histories is derived from continental erosion histories, marine stratigraphic architecture, or landscape morphology. Here we use a landscape evolution model to integrate a large dataset of low-temperature thermochronometry, sediment flux rates to surrounding marine basins, and current topography for southern Africa. We explore three main hypotheses for surface uplift: 1) southern Africa was already elevated by the Early Cretaceous before Gondwana breakup, 2) uplift and continental tilting occurred during the mid-Cretaceous, or 3) uplift occurred during the mid to late Cenozoic. We test which of these three intervals of plateau development are plausible by using an inversion method to constrain the range in erosional and uplift model parameters that can best reproduce the observed data. Results indicate four regions of parameter space that fall into two families of uplift histories are most compatible with the data. Both uplift families have limited initial topography with some topographic uplift and continental tilting starting at ~90-100 Ma. In one acceptable scenario, nearly all of the topography, >1300 m, is created at this time with little Cenozoic uplift. In the other acceptable scenario, ~400-800 m of uplift occurs in the mid-Cretaceous with another ~500-1000 m of uplift in the mid-Cenozoic. The two model scenarios have different geodynamic implications, which we compare to geodynamic models

    AtHVA22a, a plant-specific homologue of Reep/DP1/Yop1 family proteins is involved in turnip mosaic virus propagation

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    The movement of potyviruses, the largest genus of single-stranded, positive-sense RNA viruses responsible for serious diseases in crops, is very complex. As potyviruses developed strategies to hijack the host secretory pathway and plasmodesmata (PD) for their transport, the goal of this study was to identify membrane and/or PD-proteins that interact with the 6K2 protein, a potyviral protein involved in replication and cell-to-cell movement of turnip mosaic virus (TuMV). Using split-ubiquitin membrane yeast two-hybrid assays, we screened an Arabidopsis cDNA library for interactors of TuMV6K2. We isolated AtHVA22a (Hordeum vulgare abscisic acid responsive gene 22), which belongs to a multigenic family of transmembrane proteins, homologous to Receptor expression-enhancing protein (Reep)/Deleted in polyposis (DP1)/Yop1 family proteins in animal and yeast. HVA22/DP1/Yop1 family genes are widely distributed in eukaryotes, but the role of HVA22 proteins in plants is still not well known, although proteomics analysis of PD fractions purified from Arabidopsis suspension cells showed that AtHVA22a is highly enriched in a PD proteome. We confirmed the interaction between TuMV6K2 and AtHVA22a in yeast, as well as in planta by using bimolecular fluorescence complementation and showed that TuMV6K2/AtHVA22a interaction occurs at the level of the viral replication compartment during TuMV infection. Finally, we showed that the propagation of TuMV is increased when AtHVA22a is overexpressed in planta but slowed down upon mutagenesis of AtHVA22a by CRISPR-Cas9. Altogether, our results indicate that AtHVA22a plays an agonistic effect on TuMV propagation and that the C-terminal tail of the protein is important in this process.</p

    UWGeodynamics: A teaching and research tool for numerical geodynamic modelling

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    International audienceThe UWGeodynamics module facilitates development of 2D and 3D thermo-mechanicalgeodynamic models (Subduction, Rift, Passive Margins, Orogenic systems etc.). It isdesigned to be used for research and teaching, and combined the flexibility of the Under-world Application Programming Interface, (Moresi, Dufour, & MĂŒhlhaus, 2002, Moresi,Dufour, & MĂŒhlhaus (2003), Moresi et al. (2007)) with a structured workflow.Designing geodynamic numerical models can be a daunting task which often requiresgood understanding of the numerical code. UWGeodynamics provides a simple interfacewith examples to get you started with development of numerical models. Users can startdesigning their models without any pre-existing knowledge of programming. Expert userscan easily modify the framework and adapt it to more specific needs. The code can be runin parallel on multiple CPUs on personal computers and/or High Performance Computingsystems.Although UWGeodynamics has been primarily designed to address geodynamic problems,it can also be used to teach fluid dynamics and material mechanics.UWGeodynamics uses the flexibility of the Python language and the Jupyter Notebookenvironment, which allows leveraging the wide range of scientific libraries available fromthe Python community. It also facilitates the coupling with existing scientific Pythonmodules such as Badlands (Salles, Ding, & Brocard, 2018).The functionalities include:‱Dimensional input values, using user’s choice of physical units.‱Automated and transparent scaling of dimensional values.‱Sets of predefined geometries that can be combined to define the initial geometryof a model.‱Handles Newtonian and non-Newtonian rheologies (Viscous, Visco-plastic andVisco-elasto-plastic).‱Database of common rheologies used in geodynamics, which can be personalised /extended by users.‱Simple definition of kinematic, stress, and thermal boundary conditions.‱Lithostatic pressure calculation‱Thermal equilibrium (steady-state) calculation.‱Pseudo Isostasy using a range of kinematic or stress boundary conditions.‱Partial melt calculation and associated change in viscosity / heat production.‱Simple definition of passive tracers and grid of tracers.‱Simple Phase changes‱2-way coupling with the surface processes model pyBadlands (Salles et al., 2018).UWGeo comes with a series of examples, benchmarks and tutorial setups that can be usedas cookbook recipes. They provide a wide range of teaching materials useful to introducenumerical geodynamic modeling to students.New functionalities are constantly being added to the code and contributions are morethan welcomed. You can access the full documentation online athttps://uwgeodynamics.readthedocs.i
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