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Nosov, A.

Publications and source records attributed to Nosov, A..

3 recordsLinked to original sources

EBV Triggers a Distinct Antiviral Response in HMC3 Cells

Epstein-Barr Virus (EBV) is a gamma herpesvirus found in >90% of the world population that is associated with primary central nervous system (CNS) malignancy development in immunocompromised people. To provide mechanistic links between EBV infection and CNS malignancies, we investigated the capacity for EBV particles to suppress anti-tumor immunity in human microglia through a cell line model. With this approach, we exposed HMC3 cells to EBV-derived glycoprotein 350 (GP350), UV-inactivated EBV (UVi-EBV), and lipoteichoic acid (LTA) for up to 72 hours. Acute impacts of EBV particles and glycoprotein on microglial physiology were characterized at various timepoints in this model through measures of cytokine production, mRNA expression, and endocytosis. We found that UVi-EBV exposure significantly suppressed microglial production of anti-tumor interferons (IFNs) and upregulated microglial expression of the proto-oncogenic immediate early genes FOS and EGR1. Notably, there was no impairment of microglial endocytic functions following UVi-EBV stimulation, suggesting a compartmentalized suppression on IFN signaling. Overall, these findings reveal that the EBV-mediated inhibition of microglial IFN production may contribute to CNS malignancies and emphasize the urgency of innovating therapeutic strategies which target EBV to restore microglial anti-tumoral immunity. ImportanceEvidence linking EBV infection with primary CNS lymphomas and leiomyosarcomas are abundant, yet it is unclear whether EBV infection influences the CNS microenvironment and whether these effects then promote tumorigenesis. This study demonstrates evidence for EBV particle exposure to influence microglial immune phenotypes by suppressing IFN production, providing a putative mechanism for EBV virion expression in the CNS to suppress anti-tumoral immunity against EBV+ cancers. These results are particularly relevant to the etiology of EBV+ primary CNS cancers in immunocompromised people, where microglial play a heightened role in protecting the CNS in the absence of adaptive immunity.

microbiology↗

FAMOSS, a conserved 41-aa peptide involved in plant tip growth regulation

Recent evidence shows that small open reading frame (smORF; <100 codons)-encoded peptides (SEPs) containing transmembrane domains are preadapted to be progenitors of novel functional genes. A dozen of such SEPs translated from long non-coding RNAs (lncRNAs) are already functionally characterised in animals. However, functional plant lncRNA-smORF-coded peptides are not yet described. Here, we report detailed functional characterization of a 41-aa peptide encoded by lncRNA-smORFs in the moss Physcomitrium patens, which was named "FAst-growing MOSS" (FAMOSS). We found that the FAMOSS interacts with the Rab-type small GTPase proteins and its overexpression leads to faster moss growth rate and more intensive vesicular transport in apical cells, while its knockout results in the opposite effect. The FAMOSS contains a predicted transmembrane domain and possible orthologs from streptophyta algae to flowering plants have a very conserved structure. Thus, the FAMOSS peptide is a previously unknown conserved player of Rab-mediated processes in plants. Our findings are in line with functional studies of transmembrane SEPs in animals and prove the principles of SEPs evolution. This study provides new insights into functions of plant lncRNA-smORFs.

plant biology↗

The systematic assessment of completeness of public metadata accompanying omics studies

Recent advances in high-throughput sequencing technologies have made it possible to collect and share a massive amount of omics data, along with its associated metadata. Enhancing metadata availability is critical to ensure data reusability and reproducibility and to facilitate novel biomedical discoveries through effective data reuse. Yet, incomplete metadata accompanying public omics data may hinder reproducibility and reusability by reducing sample interpretability and limiting secondary analyses. In this study, we performed a comprehensive assessment of metadata completeness shared in both scientific publications and/or public repositories by analyzing over 253 studies encompassing over 164 thousands samples, including both human and non-human mammalian studies. We observed that studies often omit over a quarter of important phenotypes, with an average of only 74.8% of them shared either in the text of publication or the corresponding repository. Notably, public repositories alone contained 62% of the metadata, surpassing the textual content of publications by 3.5%. Only 11.5% of studies completely shared all phenotypes, while 37.9% shared less than 40% of the phenotypes. Studies involving non-human samples were more likely to share metadata than studies involving human samples. We observed similar results on the extended dataset spanning 2.1 million samples across over 61,000 studies from the Gene Expression Omnibus repository. The limited availability of metadata reported in our study emphasizes the necessity for improved metadata sharing practices and standardized reporting. Finally, we discuss the numerous benefits of improving the availability and quality of metadata to the scientific community and beyond, supporting data-driven decision-making and policy development in the field of biomedical research. This work provides a scalable framework for evaluating metadata availability and may help guide future policy and infrastructure development.

bioinformatics↗