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The dispersed pollution caused by microplastics (MPs) represents a current and global concern. While the fragmentation of plastic debris into smaller particles occurs in rivers, little MP research is done on freshwater species and is published compared to the marine environment. The Loire River is the longest river in France and is subject to moderate to high anthropic pressure while it represents major societal and economic issues. However, there are not many studies that have been put forward with regards to the effect of environmental MPs (EMPs) on aquatic organisms and no policies have been enacted to monitor the plastic pollution. In this study, freshwater bivalves, Corbicula fluminea, were exposed for 21 days to environmentally relevant concentrations of a mixture of <200 µm MPs generated from plastic litter collected directly along the banks of the Loire River. This mixture was composed of 40% polyethylene (PE), 40% polypropylene (PP), 10% polyethylene terephthalate (PET) and 10% polyvinylchloride (PVC) (mass percentage). Ecotoxicological effects were assessed from the individual to the molecular levels on several endpoints: condition index, filtration efficiency, enzyme activities, lipid peroxidation, energy reserves and gene expression. The ingestion of EMPs caused damages at the biochemical level. Indeed, we reported an increase in catalase activity in gills and digestive mass, a decrease in TBARs in gills, a decrease in acetylcholinesterase activity in the digestive mass, a decrease of glycogen and lipid contents in the whole organisms and a significant induction of the expression of gst, cat, mp, acp genes. The current results suggest therefore that long-term exposure to realistic doses of EMPs causes toxicity towards freshwater benthic biota. The analysis of biomarker activities and the analysis of gene expression are complementary to prevent the effects of a plastic contamination at higher biological levels in aquatic organisms.

Plastic pollution has become a global and emergency concern. Degradation processes of plastic macrowaste, either at the millimetre- and micrometre-size scales (microplastics, MP) or a nanometre one (nanoplastic, NP), is now well documented in all environmental compartments. It is hence necessary to study the environmental dynamic of MNP (micro(nano)plastic) on aquatic macrofauna considering their dispersion in different compartments. In this context, worms, having a large habitat in natural environments (soil, sediment, water) represent a relevant model organism for MNP investigations. In aquatic systems, worms could be used to compare MNP contamination between freshwater and seawater. The aim of this review was to discuss the relevance of using worms as model species for investigating MNP pollution in freshwater, estuarine, and marine systems. In this context, studies conducted in the field and in laboratory, using diverse classes of aquatic worms (polychaete and clitellate, i.e. oligochaete and hirudinea) to assess plastic contamination, were analysed. In addition, the reliability between laboratory exposure conditions and the investigation in the field was discussed. Finally, in a context of plastic use regulation, based on the literature, some recommendations about model species, environmental relevance, and experimental needs related to MNP are given for future studies. Graphical Abstract

Participants in the coastal socio-economy of the Mediterranean Sea, such as industries, aquaculture, urban populations, conglomerates, and tourists, create intense anthropogenic pressures on marine ecosystems (such as the release of trace metals). This raises concerns about their impact on the surrounding environment and on marine organisms, including those collected for human consumption. This study introduces the possibility of using Patella caerulea (Linnaeus 1758), indigenous to the Mediterranean Sea, as a biosentinel of marine pollution. This study proposes coupling environmental (bioaccumulation) and toxicological (redox homeostasis) measures of bioavailability with genetic variability (COI mtDNA) assessments. Concentrations of six trace metals (cadmium, copper, iron, lead, nickel, and zinc) were measured in surface seawater and in P. caerulea individuals collected from four coastal stations on the Tunisian coast where different levels of metal contamination have occurred. The quantified biomarkers involved the determination of antioxidant defense enzymes, catalase (CAT), glutathione peroxidase (GPX), superoxide dismutase (SOD), and the measurement of lipid peroxidation indicated by malondialdehyde (MDA) levels. Our study identified critical levels of metal contamination among locations in the Gulf of Gabes. Concomitantly, the induction of antioxidant biomarkers (especially SOD and GPX) was observed, highlighting the potential of P. caerulea to acclimate to stressful pollution conditions. Molecular analysis of COI (mtDNA) revealed low discrimination between the four P. caerulea populations, highlighting the role of marine currents in the Mediterranean Sea in the dispersal and passive transportation of limpet larvae, allowing an exchange of individuals among physically separated, P. caerulea populations.

After 20 years of assessing ecotoxicological risks of engineered nanomaterials, data gaps limit the efficacy of regulatory guidelines. Presently, there are efforts to compile historical data on nanomaterial research into online data platforms that follow FAIR (findable, accessible, interoperable, and reusable) principles. FAIR data practices for alternative testing strategies such as mesocosms are needed as standard testing strategies and regulatory platforms do not appropriately capture the mobility and bioavailability of nanomaterials in an ecosystem, limits their ability to define environmental risk. The study created a FAIR dataset for mesocosm research from three European projects with data conforming to standard ontologies modified to accommodate mesocosms. Data ranked well on the FAIRness maturity indicator proposed by the European Union’s Horizon 2020 initiative, with data on physicochemical properties being a major limitation for reusability. Statistical analysis demonstrated that chemical elements were a dominant descriptor of the data. FAIR data were achieved in the present study; however, the research highlights questions surrounding data reporting guidelines for alternative testing strategies. Considerations around data usage for historical data are also necessary to meet stakeholder needs.

Polymorphism of microsatellite markers is often associated with the simple sequence repeat motif targeted. AT-rich microsatellites tend to be highly variable and this appears to be notable, especially in legume genomes. To analyze the value of AT-rich microsatellites for common bean ( Phaseolus vulgaris L.), we developed a total of 85 new microsatellite markers, 74 of which targeted ATA or other AT-rich motif loci and 11 of which were made for GA, CA or CAC motif loci. We evaluated the loci for the level of allelic diversity in comparison to previously characterized microsatellites using a panel of 18 standard genotypes and genetically mapped any loci polymorphic in the DOR364 × G19833 population. The majority of the microsatellites produced single bands and detected single loci, however, 15 of the AT-rich microsatellites produced multiple or double banding patterns; while only one of the GA or CA-rich microsatellites did. The polymorphism information content (PIC) values averaged 0.892 and 0.600 for the AT and ATA motif microsatellites, respectively, but only 0.140 for the CA-rich microsatellites. GA microsatellites, which had a large average number of repeats, had high to intermediate PIC, averaging 0.706. A total of 45 loci could be genetically mapped and distribution of the loci across the genome was skewed towards non-distal locations with a greater prevalence of loci on linkage groups b02, b09 and b11. AT-rich microsatellites were found to be a useful source of polymorphic markers for mapping and diversity assessment in common bean that appears to uncover higher diversity than other types of simple sequence repeat markers.

Augmenting the portfolio of therapeutics for type 2-driven diseases is crucial to address unmet clinical needs and to design personalized treatment schemes. An attractive therapy for such diseases would consist in targeting the recruitment of T helper 2 (Th2) lymphocytes to inflammatory sites. Herein, we show the degradation of filamins (FLN) a and b by the ASB2α E3 ubiquitin ligase as a mechanism sustaining Th2 lymphocyte functions. Low levels of FLNa and FLNb confer an elongated shape to Th2 lymphocytes associated with efficient α V β 3 integrin-dependent cell migration. Genes encoding the α V β 3 integrin and ASB2α belong to the core of Th2-specific genes. Using genetically modified mice, we find that increasing the levels of FLNa and FLNb in Th2 lymphocytes reduces airway inflammation through diminished Th2 lymphocyte recruitment in inflamed lungs. Collectively, our results highlight ASB2α and its substrates FLNa and FLNb to alter Th2 lymphocyte-mediated responses. Filamin proteins are degraded by ASB2α E3 ubiquitin ligase and may affect T cell function. Here the authors show that increased levels of Filamin A and Filamin B in Th2 cells reduces allergic inflammation in mouse models through reduced Th2 cell recruitment into inflamed lungs.

Ubiquitin-mediated protein degradation is the main mechanism for controlled proteolysis, which is crucial for muscle development and maintenance. The ankyrin repeat-containing protein with a suppressor of cytokine signaling box 2 gene ( ASB2 ) encodes the specificity subunit of an E3 ubiquitin ligase complex involved in differentiation of hematopoietic cells. Here, we provide the first evidence that a novel ASB2 isoform, ASB2 β , is important for muscle differentiation. ASB2 β is expressed in muscle cells during embryogenesis and in adult tissues. ASB2 β is part of an active E3 ubiquitin ligase complex and targets the actin-binding protein filamin B (FLNb) for proteasomal degradation. Thus, ASB2 β regulates FLNb functions by controlling its degradation. Knockdown of endogenous ASB2 β by shRNAs during induced differentiation of C2C12 cells delayed FLNb degradation as well as myoblast fusion and expression of muscle contractile proteins. Finally, knockdown of FLNb in ASB2 β knockdown cells restores myogenic differentiation. Altogether, our results suggest that ASB2 β is involved in muscle differentiation through the targeting of FLNb to destruction by the proteasome.

Conventional dendritic cells (cDCs) comprise distinct populations with specialized immune functions that are mediators of innate and adaptive immune responses. Transcriptomic and proteomic approaches have been used so far to identify transcripts and proteins that are differentially expressed in these subsets to understand the respective functions of cDCs subsets. Here, we showed that the Cullin 5-RING E3 ubiquitin ligase (E3) ASB2α, by driving degradation of filamin A (FLNa) and filamin B (FLNb), is responsible for the difference in FLNa and FLNb abundance in the different spleen cDC subsets. Importantly, the ability of these cDC subsets to migrate correlates with the level of FLNa. Furthermore, our results strongly point to CD4 positive and double negative cDCs as distinct populations. Finally, we develop quantitative global proteomic approaches to identify ASB2α substrates in DCs using ASB2 conditional knockout mice. As component of the ubiquitin-proteasome system (UPS) are amenable to pharmacological manipulation, these approaches aimed to the identification of E3 substrates in physiological relevant settings could potentially lead to novel targets for therapeutic strategies.

ABSTRACT Osteoclasts are multinucleated cells unique in their ability to resorb bone. Osteoclastogenesis involves several steps of actin-driven rearrangements that participate not only in the cell-cell fusion process, but also in the formation of the sealing zone, the adhesive structure determining the resorption area. Despite the importance of these actin cytoskeleton-based processes, their precise mechanisms of regulation are still poorly characterized. Here, we found that moesin, a member of the Ezrin/Radixin/Moesin (ERM) protein family, is activated during osteoclast maturation and plays an instrumental role for both osteoclast fusion and function. In mouse and human osteoclast precursors, moesin is negatively regulated to potentiate their ability to fuse and degrade bone. Accordingly, we demonstrated that moesin depletion decreases membrane-to-cortex attachment and enhances formation of tunneling nanotubes (TNTs), F-actin-containing intercellular bridges that we revealed to trigger osteoclast fusion. In addition, via a β3-integrin/RhoA/SLK pathway and independently of its role in fusion, moesin regulates the number and organization of sealing zones in mature osteoclast, and thus participates in the control of bone resorption. Supporting these findings, we found that moesin-deficient mice are osteopenic with a reduced density of trabecular bones and increased osteoclast abundance and activity. These findings provide a better understanding of the regulation of osteoclast biology, and open new opportunities to specifically target osteoclast activity in bone disease therapy.