Biology subjects

Anton, A.

Publications and source records attributed to Anton, A..

5 recordsLinked to original sources

bioRxiv2025

Ecology of the exotic macroalga Batophora occidentalis in Posidonia oceanica meadows and other native benthic habitats

Marine invasive macroalgae can be particularly detrimental to native ecosystems. The exotic green macroalga B. occidentalis was first reported in 2020 in Estany des Peix lagoon in Formentera (Spain). In 2023 and 2024, our surveys revealed that B. occidentalis had spread to 100% of the surveyed locations within the lagoon. In 2024, B. occidentalis reached an average cover of 30% in Cymodocea nodosa meadows and 26% in Caulerpa prolifera meadows, with respective biomasses of 52 g m-1 and 44 g m-1, making it the most abundant macrophyte in these two native benthic habitats. We also found exotic B. occidentalis growing epiphytically on the leaves and rhizomes of Posidonia oceanica within the lagoon, with an average cover of 12% in 2023 and 16% in 2024, and a biomass of 3 g m-1 in 2024. Notably, it covered nearly 25% of the P. oceanica leaf surface and reached up to five times the weight of individual leaves. Alarmingly, we report the presence of a B. occidentalis specimen on a P. oceanica shoot in a nearby meadow outside the lagoon, signaling a potential spread beyond its current range. Additionally, B. occidentalis colonized various natural and hard substrates--including boat hulls, as it was found growing on 17 % of boats anchored in the only marina in the lagoon. With this study, we aim to encourage prompt action from local and regional governments. We may be witnessing the early stages of a broader B. occidentalis expansion, highlighting a critical moment for implementing early management measures such as monitoring, and, if possible, containment within the lagoon.

ecology↗

bioRxiv2023

Zika virus remodels and hijacks IGF2BP2 ribonucleoprotein complex to promote viral replication organelle biogenesis

Zika virus (ZIKV) infection causes significant human disease that, with no approved treatment or vaccine, constitutes a major public health concern. Its life cycle entirely relies on the cytoplasmic fate of the viral RNA genome (vRNA) through a fine-tuned equilibrium between vRNA translation, replication and packaging into new virions, all within virus-induced replication organelles (vRO). In this study, with an RNAi mini-screening and subsequent functional characterization, we have identified insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) as a new host dependency factor that regulates vRNA synthesis. In infected cells, IGF2BP2 associates with viral NS5 polymerase and redistributes to the perinuclear viral replication compartment. Combined fluorescence in situ hybridization-based confocal imaging, in vitro binding assays, and immunoprecipitation coupled to RT-qPCR, showed that IGF2BP2 directly interacts with ZIKV vRNA 3-nontranslated region. Using ZIKV sub-genomic replicons and a replication-independent vRO induction system, we demonstrated that IGF2BP2 knockdown impairs de novo viral organelle biogenesis and, consistently, vRNA synthesis. Finally, the analysis of immunopurified IGF2BP2 complex using quantitative mass spectrometry and RT-qPCR, revealed that ZIKV infection alters the protein and RNA interactomes of IGF2BP2. Altogether, our data support that ZIKV hijacks and remodels the IGF2BP2 ribonucleoprotein complex to regulate vRO biogenesis and vRNA neosynthesis.

microbiology↗

bioRxiv2023

Flaviviruses alter endoplasmic reticulum-mitochondria contacts to regulate respiration and apoptosis

With no therapeutics available, there is an urgent need to better understand the pathogenesis of flaviviruses which constitute a threat to public health worldwide. During infection, dengue virus (DENV) and Zika virus (ZIKV), two flaviviruses induce alterations of mitochondria morphology to favor viral replication, suggesting a viral co-opting of mitochondria functions. Here, we performed an extensive transmission electron microscopy-based quantitative analysis to demonstrate that both DENV and ZIKV alter endoplasmic reticulum-mitochondria contacts (ERMC). This correlated at the molecular level with an impairment of ERMC tethering protein complexes located at the surface of both organelles. Furthermore, virus infection, as well as NS4B expression modulated the mitochondrial oxygen consumption rate. Consistently, metabolomic and mitoproteomic analyses revealed a decrease in the abundance of several metabolites of the Krebs cycle and changes in the stoichiometry of the electron transport chain. Most importantly, ERMC destabilization by protein knockdown increased virus replication while dampening ZIKV-induced apoptosis. Overall, our results support the notion that flaviviruses hijack ERMCs to generate a cytoplasmic environment beneficial for sustained and efficient replication.

microbiology↗

bioRxiv2020

Naturally occurring SARS-CoV-2 gene deletions close to the spike S1/S2 cleavage site in the viral quasispecies of COVID19 patients

The SARS-CoV-2 spike (S) protein, the viral mediator for binding and entry into the host cell, has sparked great interest as a target for vaccine development and treatments with neutralizing antibodies. Initial data suggest that the virus has low mutation rates, but its large genome could facilitate recombination, insertions, and deletions, as has been described in other coronaviruses. Here, we deep-sequenced the complete SARS-CoV-2 S gene from 18 patients (10 with mild and 8 with severe COVID-19), and found that the virus accumulates deletions upstream and very close to the S1/S2 cleavage site, generating a frameshift with appearance of a stop codon. These deletions were found in a small percentage of the viral quasispecies (2.2%) in samples from all the mild and only half the severe COVID-19 patients. Our results suggest that the virus may generate free S1 protein released to the circulation. We propose that natural selection has favored a "Dont burn down the house" strategy, in which free S1 protein may compete with viral particles for the ACE2 receptor, thus reducing the severity of the infection and tissue damage without losing transmission capability.

microbiology↗

bioRxiv2020

Evolution, geographic spreading, and demographic distribution of Enterovirus D68

BackgroundWorldwide outbreaks of enterovirus D68 (EV-D68) in 2014 and 2016 have caused serious respiratory and neurological disease. MethodsWe collected samples from several European countries during the 2018 out-break and determined 53 near full-length genome ( whole genome) sequences. These sequences were combined with 718 whole genome and 1,987 VP1-gene publicly available sequences. FindingsIn 2018, circulating strains clustered into multiple subgroups in the B3 and A2 subclades, with different phylogenetic origins. Clusters in subclade B3 emerged from strains circulating primarily in the US and Europe in 2016, though some had deeper roots linking to Asian strains, while clusters in A2 traced back to strains detected in East Asia in 2015-2016. In 2018, all sequences from the USA formed a distinct subgroup, containing only three non-US samples. Alongside the varied origins of seasonal strains, we found that diversification of these variants begins up to 18 months prior to the first diagnostic detection during a EV-D68 season. EV-D68 displays strong signs of continuous antigenic evolution and all 2018 A2 strains had novel patterns in the putative neutralizing epitopes in the BC- and DE-loops. The pattern in the BC-loop of the USA B3 subgroup had not been detected on that continent before. Patients with EV-D68 in subclade A2 were significantly older than patients with a B3 subclade virus. In contrast to other subclades, the age distribution of A2 is distinctly bimodal and was found primarily among children and in the elderly. InterpretationWe hypothesize that EV-D68s rapid evolution of surface proteins, extensive diversity, and high rate of geographic mixing could be explained by substantial reinfection of adults. FundingUniversity of Basel and Swedish Foundation for Research and Development in Medical Microbiology

microbiology↗